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Oral finasteride, a type II 5-alpha reductase inhibitor, is one of the most effective treatments available for androgenic alopecia (AGA). However, concerns over the drug’s potential side effects prevent many men from ever considering the medication.

In the last several years, nearly a dozen studies have shown that certain formulation topical finasteride may confer the same hair growth-promoting benefits as oral finasteride, but with less systemic drug exposure. For those worried about side effects, topical finasteride is often a stepping stone toward an effective treatment protocol for hair regrowth.

In this article, we’ll uncover how to make topical finasteride using crushed pills – which is perhaps the least expensive alternative to DIY topical finasteride. We’ll also explain why doing so might be short-sighted, and that there is likely a better way to reduce costs for topical finasteride, but also control for the quality of the product: diluting topical finasteride that is already purchased.

Interested in Topical Finasteride?

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

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

Why Make Topical Finasteride at Home? 

Most people consider making DIY topical finasteride for two reasons:

1. Cost savings. Compounding pharmacies often charge $50-$100 per month for topical finasteride, thus pricing out a lot of men and women who would otherwise be interested in trying it. However, oral finasteride prescriptions are often 2-5 times cheaper on a monthly basis. This has led many to wonder, “Why don’t I save money by crushing my finasteride pills into a solution and apply that topical directly on my head?” While there are cost-savings behind this logic, the actual step-by-step process is a little more involved (more on this later).
2. Control over dilutions. Most big-brand formulations of topical finasteride use dilution percentages that actually expose users to more finasteride each day than if they were to use the drug orally. For instance, Hims sells a 0.3% topical finasteride solution, of which many customers will apply 1 mL daily or more to cover all balding regions. That actually equates to 3 mg of finasteride exposure daily, which is 3 times the amount of drug prescribed daily for oral consumption (i.e., 1 mg). Under these circumstances, if just 0.2 mg of that topical drug escapes the scalp skin and enters the bloodstream, most users will experience the same systemic hormonal modifications as if they were to instead just use the oral medication.

To elaborate on that second point, just see this chart below, which shows just how little finasteride needs to be consumed to affect serum levels of dihydrotestosterone (DHT).

With that in mind, see this other cart, which shows topical finasteride’s effects on serum DHT – a proxy to estimate systemic drug exposure – while controlling for the daily exposure (in mg) of finasteride applied to the scalp. The higher the daily dose, the higher the systemic reductions to DHT.

For these reasons, many topical finasteride users prefer to have the ability to titrate their daily dosages of the topical. They can do this by:

1. Using less of the topical finasteride solution. The shortcoming: with less solution, you may not be able to apply the topical to all balding regions.
2. Using topical finasteride fewer days per week. The shortcoming: this throws off the rhythm of a daily routine, and at a certain threshold, reduces efficacy.
3. Making their own topical finasteride. The shortcoming: it takes additional work, and it’s not always clear if you did it right.

Moreover, a lot of people presume that making their own topical finasteride is as simple as crushing their own prescription of finasteride pills into water, then applying that directly to the scalp. It isn’t.

Nonetheless, most people opt for option #3: making their own topical finasteride. And most people prefer to do this by crushing pills. While we strongly recommend getting properly formulated topical finasteride prescribed to you and made by a compounding pharmacy, for those who don’t heed this advice and instead go with the pill-crushing approach, here are some educational resources (and a free calculator) that might help you.

Making Topical Finasteride By Crushing Pills: Step-By-Step Instructions

Before proceeding, it’s important to recall what your goals are for opting to try topical finasteride. In 99% of cases, it’s going to be to minimize the risk of adverse events while maximizing the chances of growing new hair. If that is your goal, consider the following.

1. Settle on a daily dose of finasteride exposure

Serum DHT reductions act as proxies for estimate systemic absorption from topical finasteride, and thereby the risk of side effects. On that note, the only clinically studied formulation of topical finasteride that (1) demonstrated effectiveness in men and women, and (2) led to no changes in serum DHT, is one that exposed participants to ~0.1 mg daily of topical finasteride. That’s 1/10th the amount of the standard oral dose prescribed for androgenic alopecia.

This dose of topical finasteride is typically applied daily in the following formulas:

• 0.01% at 1 mL daily – good for those with localized hair loss
• 0.005% at 2 mL daily – good for those with diffuse hair loss (more topical to spread across the scalp)

So, for those who want to be as cautious as possible, this is probably the dose that is most appropriate to start for topical finasteride. Higher doses also work, and also still likely confer a reduction in side effect risk, but at the expense of guaranteed DHT reductions elsewhere in the body. With the 0.1 mg low-dose formula, this risk (according to the clinical literature) is a lot lower.

2. Consider your carrier ingredients

Carrier ingredients help carry a topical’s active ingredient into deeper layers of the skin, where it can have its desired effects. In the case of topical finasteride, carrier ingredients help bring finasteride through the stratum corneum and into the mesodermal sheath, outer root sheath, and dermal papillae cell clusters of hair follicles – where the drug can get to work inhibiting type II 5-alpha reductase and lowering scalp levels of DHT.

When it comes to topical finasteride, some carrier ingredients work better than others at enhancing skin penetration. For an example, see this chart:^[1]https://ncbi.nlm.nih.gov/pmc/articles/PMC2977015/

 

There are a few key takeaways from this chart:

1. Topical finasteride’s penetration into the skin is linear across 4 common carrier agents. That means the longer you leave in the topical without washing your hair, the more of it will absorb into the skin.
2. This enhanced skin penetration will also come at the expense of higher systemic absorption of the drug. For these reasons, we recommend serum DHT testing regularly with topical finasteride. Our membership has resources on how to do this, and we can team members and researchers who will personally support you through this entire process if you need it.
3. Don’t just mix your finasteride pills with water. As we can see from the chart, water is a terrible carrier ingredient for topical finasteride.

In our topical finasteride calculator (it’s free), we recommend a series of low-cost carrier ingredients for you, as well as links to the actual products. Please note: we do not receive commissions on any of those product recommendations, as doing so would undermine the objectives of this site: to be as unbiased as possible in our scientific analyses (and advice) to hair loss sufferers.

3. Before crushing your finasteride pills, remove any pill coatings

Depending on where your finasteride pills were manufactured, there’s a strong likelihood that the pills come with a protective coating that prevents incidental drug exposure from anyone who might’ve handled the drug without the intention of ingesting it. This is generally to prevent pregnant women from coming into incidental contact with the drug.

As such, if you’re going to use your prescribed finasteride pills to make topical finasteride, it’s critical to remove this protective coating from each pill in order to allow those pills a better chance at dissolving into the topical solution. You can do this by scraping the pills with a small knife or nail clipper, and then peeling off all of the coating with your finger tips.

4. Use our topical finasteride calculator to dial in your DIY, homemade topical finasteride formulation

The math involved in making topical finasteride isn’t likely solving an equation for quantum physics. At the same time, it’s also not as straightforward as many people would like. After all, you have to account for the following:

1. Hair loss patterning (localized vs. diffuse) – as this determines if you’ll need 1 mL or 2 mL of liquid daily to cover all balding regions
2. Dilution amounts – which, together with the mL of daily application, will determine your daily total finasteride exposure
3. Adjustments for pill sizes (in mg). After all, oral finasteride pills are available in 1 mg and 5 mg daily doses, so you’ll need to account for this prior to crushing anything

To take the guesswork out of this process, we decided to do all of the math for you. Then we hired developers to integrate these math equations into an interactive survey that factors in all of the above, then spits out step-by-step instructions for how to make topical finasteride by crushing pills.

You can access the topical finasteride calculator right here. It’s 100% free.

To reiterate, this calculator is not medical advice and is for educational purposes only. We still strongly recommend that you just get your topical finasteride properly formulated by a compounding pharmacy. Nonetheless, the calculator is there for those who decide to ignore this advice and instead take the cost-savings route toward topical hair loss treatments.

Final Thoughts

We produce content like this to benefit hair loss sufferers worldwide – regardless of their financial circumstances. With more access to free information, more men and women can seek effective hair loss treatments faster, and thereby improve their outcomes long-term.

With that said, these free resources represent just a tiny fraction of what’s available inside our membership community. If you’re looking for personal support on your hair growth journey, interactions with hair loss researchers, one-on-one video calls, and a customized hair growth protocol built around your needs, preferences, goals, and the evidence – our membership is the place where we offer these services.

It’s also the way in which we monetize this site, which is why we’ve never accepted any hair loss product advertisements or commissions – which otherwise comes with the risk of biasing our own research lens and interpretation of data. For evidence of how big this problem is, just take a look all of the other sites, forums, and YouTube personalities catering their content toward the sale of physical products to which they’re financially tied – which only serves those creators and, simultaneously, overwhelms the ecosystem of information accessible to consumers with biased advice.

Not a member of the Perfect Hair Health Membership Community? Join today to create a customized regrowth roadmap and gain access to hundreds of resources, including treatment guides, product reviews, expert interviews, forums, and more.

Topical finasteride is an effective treatment for androgenic alopecia – particularly for those interested in better localizing the drug’s effects to the scalp. Unfortunately, prescriptions for topical finasteride can cost as much as $50-$100 per month.

This prices out a lot of people who would’ve otherwise committed to the topical had it not been for its costs. It’s also led others to ask, “Can I make topical finasteride at home? Can’t I just crush up my finasteride pills or dilute another topical finasteride?”

The answer to each question is yes, with caveats. While topical finasteride can be made at home – and at a low cost – anyone who intends to try this must formulate the product properly. This might entail:

1. Removing the coating of finasteride pills prior to crushing them
2. Matching carrier agents when diluting already-existing topicals
3. Knowing how much finasteride to add to a formulation to maximize scalp DHT reductions while minimizing the risk of systemic absorption.
4. Adjusting finasteride dilutions to control for total daily drug exposure, particularly for those with diffuse vs. localized hair loss.

In this article, we’ll reveal a step-by-step process for how to make topical finasteride – either by crushing finasteride pills or diluting an already-purchased topical. We’ll also provide a topical finasteride calculator that automatically calculates step-by-step instructions for you, all depending on your desired dilutions and starting ingredients. It’s also 100% free. See below.

Interested in Topical Finasteride?

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

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

Click Here For 15% Off

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

Oral Finasteride: Efficacy & Side Effects

Oral finasteride is an effective FDA-approved drug used to treat androgenic alopecia (AGA). It reduces a hormone known as type II 5-α dihydrotestosterone (DHT) – which is causally linked to the balding process. Between 0.2 mg to 1.0 mg of finasteride daily can lower DHT levels by 70%, which is enough suppression to therapeutically improve AGA outcomes in 80-90% of male users in two years.^[1]https://www.sciencedirect.com/science/article/pii/S0022202X15529357

While most men and women tolerate finasteride without issue, clinical studies consistently show that finasteride adversely impacts a small portion of users. Between 5% to 15% of men trying the drug report mild-to-moderate side effects ranging from diminished libido to brain fog. This is because finasteride does not just reduce DHT in scalp levels, but also across all other tissues in the body such as the brain and testes. For a portion of men and women, DHT reductions of this magnitude across all body tissues can cause undesired effects.

Topical Finasteride: Is It Still Effective? Does It Have A Better Safety Profile?

To reduce the risk of side effects from oral finasteride, many people opt to try finasteride delivered topically. After all, clinical studies demonstrate that compared to 1 mg daily of oral finasteride, daily use of 1 mL x 1% topical finasteride is “non-inferior” to the oral formulation.^[2]https://pubmed.ncbi.nlm.nih.gov/19172031/

With topical delivery, users often believe that since they are isolating finasteride to the scalp skin, they can expect less finasteride to reach other parts of the body – thereby preserving DHT levels in other organ sites beyonds the scalp and lowering their risk of side effects.

But is this true?

On the one hand, clinical studies corroborate that some formulations of topical finasteride appear to reduce the risk of side effects versus oral finasteride. On the other hand, the dose per mL of topical finasteride influences this risk – as does the amount of topical finasteride applied daily along with the carrier ingredients used inside the topical formulation.

1. Daily Drug Exposure & Influence On Systemic Absorption

We can use reductions in blood levels of DHT as a proxy to estimate how much topical finasteride leaks from the scalp tissues into the blood stream, thereby traveling to other parts of the body and potentiating DHT reductions other organs.

For reference, see the following chart which summarizes clinical studies on topical finasteride in relation to its impact on DHT levels in the blood. Keep in mind that all daily exposure volumes of topical finasteride in this chart were clinically effective at improving hair. On the y-axis, we have the total daily exposure of finasteride (in mg) as a topical. On the x-axis, we show reductions to serum DHT, which acts to estimate the amount of systemic exposure of the drug (even when applied topically).

As we can see, according to the clinical literature, the only daily exposure volume of topical finasteride that improves hair loss but does not impact serum DHT levels is 0.005% x 2 mL of topical finasteride daily, which equates to just under 0.1 mg daily of finasteride applied to the scalp.

Therefore, if you intend to make topical finasteride at home with the goal of (1) improving hair loss while (2) minimizing systemic drug absorption, consider finasteride formulations of ~0.1mg daily. At higher daily doses, you can still achieve hair regrowth, but this might come at the expense with more systemic drug absorption and thereby a higher risk of side effects.

2. Carrier Agent Influence On Systemic Drug Exposure

Beyond the daily drug exposure of topical finasteride, the carrier agents used in a topical finasteride formulation also impact the amount of drug absorbed into the skin, and consequently the blood stream.

The outermost layer of the scalp’s epidermis is known as the stratum corneum. This skin layer acts as a barrier for what can enter the skin, and what can escape. It’s also a critical barrier of protection for human survival. Without a stratum corneum, human skin would absorb much more of the outside world – i.e., any nutrients, viruses, microorganisms, and/or pollutants we touch – and we’d be at a much higher risk of exogenous threats.

Unfortunately, the stratum corneum also creates a challenge for topical drug delivery. So, to bypass the stratum corneum, product formulators often add what are called “carrier ingredients” to a topical in order to allow for that topical’s active ingredients to penetrate beyond this layer and deeper into the skin — where that active ingredient can reach target areas and have a therapeutic effect.

Some common carrier ingredients are:

• Alcohol
• Propylene glycol
• Liposomes

But not all carrier ingredients are equally effective at their job. Depending on the active ingredient of a topical, some carrier ingredients do a better job than others at carrying a drug into deeper layers of the skin.

This is particularly true for topical finasteride. Just see this chart from an in vitro study measuring topical finasteride absorption across a 24-hour period, controlling for different carrier agents: ethosomes, hydroethanolic acid, liposomes, and water:^[3]https://ncbi.nlm.nih.gov/pmc/articles/PMC2977015/

Keep in mind: the more finasteride that permeates into skin tissues, the more finasteride will absorb into the blood stream. Therefore, it is critical to be aware of this relationship when formulating your own topical finasteride at home.

Moreover, if you are diluting topical finasteride from a pre-existing topical, you must ensure that the carrier ingredients used in your new formulation match those used in the already-purchased topical. For instance, if your pre-purchased prescription of topical finasteride uses a liposomal base – which is a gel – but you’re trying to dilute that gel into a liquid formulation (with propylene glycol), the formulations won’t mix well, and you’ll just be wasting product.

How To Make Homemade Topical Finasteride

Here’s a recap of key factors to consider before opting to make topical finasteride at home:

• Control for daily drug exposure. Topical finasteride can still leak into the blood stream, and at higher daily doses, the effects of serum DHT can be as dramatic as if we were using oral finasteride. Formulations greater than 0.1mg daily appear to appreciably lower scalp DHT levels, but also serum DHT levels. With exposure volumes of 1.0 mg daily and higher, serum DHT can become reduced to the same level as oral finasteride.
• Control for daily application volume. Compared to people with localized hair loss (i.e., only temple recession and/or crown thinning), those with diffuse hair loss have a much larger area affected by pattern hair loss, and will thereby need to apply more topical (in mL) versus those with smaller areas of hair loss. Under these circumstances, finasteride dilutions may also need to be titrated in order to maintain a consistent daily exposure volume of the drug. For instance, if we want to keep total topical finasteride exposure consistent at 0.1mg daily, people with localized hair loss may only need 0.01% x 1 mL formulations, whereas those with diffuse hair loss may need to titrate their dilution to 0.005% x 2 mL in order to keep daily drug exposure constant while enabling an extra mL of liquid to cover all areas regions affected by hair loss.
• Select the right carrier ingredients. Different carrier ingredients have different capacities to bring finasteride through the stratum corneum. Over 24-hour penetration periods, one study found that topical finasteride formulated with ethosomes or hydroethanol outperformed formulations of liposomes or water. Having said that, better skin penetration also comes with higher rates of systemic absorption of finasteride into the blood stream.
• If making topical finasteride by diluting a pre-purchased topical, match the carrier ingredients. If you plan on diluting a pre-purchased topical finasteride, it is critical to match carrier ingredients between the old and new formulations.
• If making topical finasteride by crushing up oral pills, peel off any pill coatings prior to crushing. Failure to do this may resort in unwanted debris in your topical formulation and an incomplete dissolution of the finasteride pills in your topical.

If these factors feel overwhelming to control for, we completely understand. For these reasons, we decided to work with developers to build an interactive calculator that generates step-by-step instructions for you to make topical finasteride calculator.

DIY Topical Finasteride: Use Our Free Topical Finasteride Calculator

The following topical finasteride calculator not only controls for daily drug exposure, topical formulations, and carrier ingredients, but it also generates step-by-step instructions for your formulation based on whether you intend to make topical finasteride by crushing finasteride pills or by diluting an already-purchased topical.

Access the free topical finasteride calculator right here.

We hope it helps!

When Homemade Finasteride Is Not Recommended

Technically speaking, making DIY topical finasteride is never advised. After all, finasteride is a prescription drug, and prescription drugs require careful manufacturing and dosing control from compounding pharmacies.

For these reasons, if you’re not so price sensitive, it’s best to leave topical finasteride formulating to the professionals and take yourself out of the equation. Otherwise, you open yourself up to the risks of improper dosing and/or inadvertently exposing others in your household to a drug they never intended to use in the first place.

So, consider getting a prescription of topical finasteride from a dermatologist or telehealth company as your first (and only) option.

Nonetheless, we also recognize that people are going to do whatever they want to do, and that despite us strongly recommending against DIY topical finasteride, people will do it anyway. While this page (and the calculator) are for educational purposes only, and while we obviously recommend seeking medical advice before doing anything, we hope that the resources here help guide those who are making topical finasteride toward doing so as safely and effectively as possible.

Final Thoughts

While we don’t recommend making topical finasteride at home, we also recognize that DIY topical finasteride can save consumers money, enable better control over daily drug exposure, reduce systemic DHT reductions, and lower the risk of adverse events associated with the drug.

Users can make topical finasteride by crushing pills or diluting pre-purchased topical finasteride. Our 100% free calculator can generate step-by-step instructions for you.

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In the medical literature, it’s well established that women should withdraw from finasteride prior to conceiving, or abstain from finasteride throughout pregnancy and/or while breastfeeding. But what about men? Can they continue using finasteride during conception? What about during their partners’ pregnancy — when indirect finasteride exposure (via semen) might expose the female and fetus to the drug?

The answers and evidence aren’t so straightforward. Fortunately, for those concerned of adverse effects from finasteride on either sperm parameters or developing fetuses, there are strategies to mitigate these risks and continue protecting your hair. This article discusses the data, and elucidates a finasteride dosing strategy for men looking to keep their hair while also growing their family.

Interested in Oral Finasteride?

Oral finasteride & minoxidil available, if prescribed*

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

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

Is it Safe for Women to Use Finasteride During Conception?

Probably not. Here’s why.

Drugs like finasteride and dutasteride can bypass the placenta, where they can begin to inhibit 5-alpha reductase activity in a developing fetus and interfere with their hormonal profile.^[1]https://rep.bioscientifica.com/configurable/content/journals$002frep$002f155$002f3$002fREP-17-0380.xml The hormone that these drugs reduce — dihydrotestosterone — is less relevant in adulthood, but is critical for early development — particularly for males. Subsequently, animal studies have shown that prolonged finasteride use in pregnant females may mutate and/or inhibit the development of male fetus genitalia.^[2]https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=f96c6acd-4d02-4ece-bd54-2d5a35aab7f5#section-12.2

Since it takes ~30 days for finasteride to clear the body, doctors recommend that women trying to conceive should discontinue the drug at least one month before conception. Some doctors even advise their pregnant female patients to avoid any finasteride exposure whatsoever — including any handling of the medication. This is out of an abundance of caution for the safety of the developing fetus.

What About Men? Can Men Use Finasteride During Conception?

When it comes to men using finasteride during windows of conceptions opinions on whether or not to discontinue the drug are split.

Most providers recommend that men stop using finasteride for at least one month prior to conceiving. Other doctors claim that quitting finasteride is unnecessary, and come at the expense of lost hair. They even go so far as to say there’s “no evidence” that finasteride use for men during windows of conception leads to different health outcomes for their future offspring.

So, which position holds more merit? We’ll detail both sides of the scientific argument below and provide our own take on the data. Then, we’ll reveal a strategy men can employ to temporarily quit finasteride — within a window that shouldn’t compromise any hair gains — and use that window to conceive without (hopefully) losing additional hair.

It all boils down to the length of time it takes for finasteride’s hair growth-promoting effects to wear off versus the length of time the medication takes to clear from the system. Fortunately, there’s a difference here that is in favor of a reproductive window.

Should Men Stop Using Finasteride Before Or During Conception?

In one research article 2001, a group of family physicians examine the perceived versus realized risk of men using oral finasteride during windows of conception.^[3]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2018472/pdf/11785276.pdf

First, the authors review evidence surrounding just how much of a daily 1mg finasteride pill ends up detectable in semen:

“In one study, semen levels were measured in 35 men taking 1 mg of finasteride daily for 6 weeks. Highest level measured was 1.52 ng/mL; mean level was 0.26 ng/mL.”

Then, the authors sought to use these numbers to estimate the total exposure of finasteride to a developing fetus — throughout a pregnancy — due to daily unprotected sex.

“Assuming a 100% vaginal absorption through a 5-mL ejaculate per day, women would be exposed to 7.6 ng/d, a negligible amount.”

Finally, the authors contextualized that risk by comparing that exposure level of finasteride to the amount that was required to cause birth defects in monkey studies.

“This level is 750 times lower than the “no effect” level for developmental abnormalities in rhesus monkeys.”

For these reasons, the authors conclude that finasteride use — at least in men — probably doesn’t need to be stopped during pregnancy.

The authors go on to state that, at least for men, the major risk of using finasteride during conception might instead be the drug’s temporary reductions to semen counts, which may impact the ability to conceive, but not the actual health of the baby (more on this later). Thus, while on finasteride, it may be more difficult to conceive within the first few months of using finasteride (when sperm parameters decline) if a male has borderline-low semen levels prior to starting the medication.

Beyond this, the authors seem far less concerned about about finasteride’s effects on the actual conception, such as potential congenital disabilities or risks to male fetal development. In fact, they assert that there’s no data that, during conception, the use of finasteride (for males) interferes with reproductive or fetal outcomes. They recommend that men taking oral finasteride keep taking the drug throughout conception.

Unfortunately, this review was conducted in 2001 — when epigenetics was still an emerging field, and when research groups weren’t necessarily aware of other markers worth measuring that might affect the health of fetal development. Today, in order to completely quell concerns of conception windows and finasteride use in men, what we really need to know is:

• Does finasteride use affect sperm parameters in men?
• Is finasteride use associated with epigenetic and/or DNA damage in sperm, and at doses prescribed for androgenic alopecia?
• Are there actual prospective, long-term studies measuring the outcomes of children whose fathers were using finasteride when they were conceived?

In exploring the answers to these questions, we’ll realize the whole debate over finasteride’s use in men during conception is not as clearcut as it may seem.

Finasteride Use In Men While Conceiving: Affect On Children (Unstudied!)

First, it is true that there are no prospective clinical studies tracking birth outcomes across men using vs. not using finasteride compared to (1) their success with conception, and (2) the health of their offspring. So, does that mean we should assume using finasteride as a male — during conception — is safe?

No. It simply means the question hasn’t been studied. Given that the life and health of a newborn is at stake, our position is that it’s probably better to exercise caution than it is to presume the absence of evidence is a signal suggesting that a behavior that has not been adequately studied must be safe.

Secondly, there’s newer data (from later than 2001) suggesting that finasteride may do more than temporarily lower the ability for men to reproduce via reduced sperm counts, and that these changes may come with a heightened risk of reproductive health.

Finasteride Use In Men: Affect On Sperm Parameters (Studied)

The effects of finasteride use on sperm parameters has been studied in humans at doses of 1-5mg. Here’s what the evidence says.

Overstreet et al (1999)

A 1999 study tested the effects of 1mg finasteride daily on sperm parameters in men. After one year, those using finasteride had an 11% decline in ejaculate volume, compared to 8% in the placebo group. The researchers also noted no significant changes to “sperm concentration, total sperm per ejaculate, sperm motility or morphology.” Resultantly, the team concluded that 1mg daily finasteride use “does not affect spermatogenesis of semen parameters” in men.^[4]https://pubmed.ncbi.nlm.nih.gov/10492183/

Given that the study was randomized, double-blinded, placebo-controlled, used the standard dose of finasteride for androgenic alopecia, and ran a full year — many people use this study as justification that finasteride use (in men) probably does not have deleterious effects on reproduction.

Unfortunately, there are two problems with this reasoning.

The first problem is that the study doesn’t actually measure reproductive outcomes, nor does it measure epigenetic changes to sperm. Rather, the study only measure changes to sperms’ histological features: its concentration, sperm per ejaculate, sperm motility, sperm morphology, and semen volume. From a safety perspective, the clinical results are a positive signal. But without long-term studies on fetal outcomes for men using finasteride during conception, they don’t actually answer the question of whether finasteride use in men affect the way their offspring develop.

The second problem is that there are other studies on finasteride that add nuance to finasteride’s safety on sperm parameters — particularly at 5mg doses.

Amory et al (2007)

A 2007 study tested the effects of daily use of 5mg finasteride or 0.5mg dutasteride on semen parameters in healthy men versus placebo. Over six months, the authors found that daily doses of 5mg of finasteride or 0.5mg of dutasteride significantly reduced sperm counts, and by 25-35%. However, at the 12-month mark of continued use, sperm counts for finasteride were still below baseline (i.e., -14.5%), but no longer statistically significantly lower than when the study began.^[5]https://academic.oup.com/jcem/article/92/5/1659/2598215

For these reasons, some researchers claim that the effects of finasteride on sperm parameters — if any — are temporary and resolve with continued use at 5mg daily doses, if those changes even exist at all at lower doses (i.e., 1mg).

This should be the end of the story, right? After all, most men are prescribed finasteride at 1mg daily for androgenic alopecia. So, if at 1mg daily there appears to be no effect on sperm parameters, and at 5mg daily the effect seems to diminish with continued use, then men must be in-the-clear to use finasteride while conceiving. Correct?

No.

Again, there are no randomized controlled clinical trials measuring long-term outcomes of children whose fathers were using finasteride before/during their conception. Moreover, sperm counts, motility, and morphogenesis are all histological features of sperm. What isn’t measured in these study is the effect of DNA expression on sperm (i.e., epigenetics). Keep in mind that you can have plenty of sperm that looks healthy, swims effectively, appears normal… but still carries with it genetic expressions that insinuate damage or a heightened potential of birth defects for the fetus.

So, is there any data giving us insights into the potential for finasteride to cause epigenetic changes to sperm (or damage to sperm) that might otherwise affect reproductive capacity and/or fetal outcomes? And no, we’re not talking mouse models that administer high-dose finasteride (which aren’t always applicable to human research, despite what hair loss forums may tell you).^[6]https://www.mdpi.com/1467-3045/43/2/62 We’re talking about human evidence.

Yes, there is evidence. And while that evidence isn’t high-quality, it’s still worth discussing.

Finasteride And Infertility In Men: Tu HY, Zini A. (2011), Şalvarci A, Istanbulluoğlu O. (2012)

In 2011 and 2012, two separate case reports were published — each on a male using finasteride long-term who was having trouble conceiving with his respective partner.

Researchers examined sperm morphology — as the studies above did — which appeared normal. But then they examined the sperm through another endpoint: a sperm DNA fragmentation index. This is a measurement to approximate DNA damage (i.e., fragmentation). In both cases, sperm DNA fragmentation was elevated. After discontinuing finasteride, one case report saw sperm DNA fragmentation reduced from 30% to 16.5% within six months.^[7]https://pubmed.ncbi.nlm.nih.gov/21292254/ The other case report noted similar improvements to DNA fragmentation, and the successful conception of a baby after discontinuing the drug.^[8]https://pubmed.ncbi.nlm.nih.gov/23070721/ The implication: that finasteride use in some men may damage the DNA of sperm, and that discontinuing the drug can improve these outcomes.

Please note: these are case reports, and with such uncontrolled (and unrobust data), there is always the possibility that something aside from the discontinuance of finasteride might be explaining these results. For instance, upon receiving this news, both men featured in the case reports might not have only stopped finasteride, but also addressed other aspects of health to reduce their risk of sperm DNA fragmentation. Examples include supplementing with vitamin D, incorporating more daily activity into their lives, quitting alcohol, getting more consistent sleep, etc.

As such, there’s always the possibility that finasteride was not the majority causative agent in either outcomes.

Our Perspectives: Should Men Continue Using Finasteride While Trying To Have a Baby?

Given the balance of evidence, we feel that men using finasteride should perhaps exercise caution about continuing the drug while also trying to grow their families.

Unfortunately, this position puts many men in an uncomfortable situation. They might feel as though they need to withdraw from a hair-saving drug in order to minimize risks that aren’t necessarily clear, based on the clinical data. Again, those long-term studies on children whose fathers conceived them while using finasteride haven’t yet occurred. They may never occur.

At the same time, this “abundance of caution” comes at a tall expense: lost hair. After all, clinical studies show that after quitting finasteride, any hair that was preserved by the drug is lost and, soon after, hair loss continues at its normal rate.

These risks-benefits are not ours to make for anyone. We’re just here to communicate the data, and the debate. Risk tolerances vary depending on the person, and for many couples, the continued use of finasteride might be the decision made by the male during the windows of conception. This is a decision that shouldn’t be made by us; it should be made by you along with the counseling of your doctor(s).

Nonetheless, if you are looking for an approach to minimize the risks to a developing fetus while simultaneously preserving hair, there is a happy middle ground… and perhaps a way to get the best of both worlds.

Consider Quitting Finasteride Temporarily During Conception

Finasteride is a drug that has a terminal half-life of 5-7 hours, and a biological half-life of around two weeks. In other words, while it takes 5-7 hours for half of the finasteride in your bloodstream to metabolize, it takes 2+ weeks for half of the effects from finasteride use — i.e., the lowering of dihydrotestosterone — to go away. For these reasons, it is estimated that after quitting finasteride, it still takes ~30 days for finasteride (and its effects) to completely leave the body.

This is why most physicians recommend beginning trying to conceive after 30+ days away from finasteride (if female). But after quitting finasteride, how long does it take before hair loss starts to pick back up again?

According to the clinical literature, longer than four weeks. In fact, one study showed that, after one full year of use, men who quit finasteride were still above their baseline hair counts a year after leaving the medication.^[9]https://www.sciencedirect.com/science/article/pii/S0022202X15529357 Another study showed that after one year of finasteride use, men who switched to every-other-month of daily medication had the same hair growth outcomes as men who still used the drug every day of the year.^[10]https://pubmed.ncbi.nlm.nih.gov/15319158/

Taken together, these studies imply that finasteride’s terminal and biological half-lives might enable a key window whereby men can transition off the drug, conceive without detectable levels of finasteride in their sperm (and/or any adverse effects on sperm from finasteride use), then hop back on the drug — all with little (if any) risk to their hair.

Based on the current data, this window appears to be 1-3 months after quitting finasteride. Within that time, hair loss from withdrawal of the drug should be relatively minimal. And with a two-month reproductive window, this should hopefully be enough time to give couples a good chance to conceive.

What About Topical Finasteride?

For women, the use of topical finasteride within a month before conceiving, during pregnancy, or while breastfeeding is not recommended. This is because a portion of the drug will still go systemic, thereby potentiating adverse events to the developing baby.

For men, there is not yet any data to answer this question — but out of caution, many physicians will just say, “Don’t do it” However, it’s likely that the risks with topical finasteride — especially at lower exposure volumes (0.1 mg daily) — are much smaller than any risks with the oral formulations of the drug (due to less systemic exposure and thereby lower concentrations in the semen).

That said, for those using topical finasteride while starting a family, the Perfect Hair Health team recommends doing everything possible to minimize topical finasteride exposure to a partner while they are pregnant. We’ll have articles on how to do this in the near-future.

What’s the Prevalence Of Sexual Side Effects From Finasteride?

Does finasteride lower libido? The true incidence of the sexual side effects of finasteride remains up for debate. Finasteride is the world’s best-studied hair loss drug. Over the past 30 years, it has been clinically tested in over 30,000 men – with dozens of randomized, double-blinded, placebo-controlled studies converging on relatively consistent efficacy and safety profiles.

While finasteride is generally well-tolerated, some users have reported sexual side effects after starting the drug. These reports are well documented in the clinical literature. However, their prevalence varies greatly depending on the study referenced.

In well-controlled clinical studies lasting 1-5 years, the incidence of these reports is generally under 7%, with 3-4% of people in the placebo group (sugar pill group) also reporting reductions to libido.^[1]https://pubmed.ncbi.nlm.nih.gov/30206635/ In fact, one randomized, double-blinded, placebo-controlled clinical trials in ~2,000 men showed – over one year – that 1 mg daily of finasteride led to reduced libido in 1.8% of users versus 1.3% in the placebo group.^[2]https://www.sciencedirect.com/science/article/pii/S0022202X15529357

This seems to indicate the risk of sexual side effects from finasteride is very low. However, other (smaller) clinical studies have put the incidence of sexual side effects as high as 25-30%. It is important to note that these smaller studies are generally of lower quality, so their results should be interpreted with caution.^[3]https://pubmed.ncbi.nlm.nih.gov/17655657/ Nonetheless, these studies and the side effects they mention do exist.

Having combed through nearly all the available literature on the subject, we estimate the true incidence of noticeable sexual side effects for finasteride users likely hovers around 3-15%.

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Why Does It Seem Like Everyone Online Says Finasteride Lowers Libido?

While side effects from hair loss drugs do occur, their perceived prevalence is often overstated on natural health websites and online forums. There are (at least) two reasons why:

• Financial incentives. Many natural websites fearmonger over hair loss drugs because they want to sell people natural alternatives – supplements and serums – that they claim are free of sexual side effects (which often isn’t true).
• The “Yelp Effect”. The Yelp Effect explains why a restaurant is far more likely to receive reviews from patrons who are dissatisfied (rather than happy) with their experience. Anger motivates us to take action more than contentment does. The same applies to FDA-approved drugs on hair loss forums (especially in online spaces like HairLossTalk and Reddit, where anonymity is preserved).

Can We Reduce the Risk of Finasteride’s Sexual Side Effects?

Yes. There are strategies to potentially reduce the risk of finasteride’s sexual side effects, while also still regrowing hair. These strategies include the following:

• Reduce the dose. As a hair loss drug, finasteride is typically prescribed orally at 1mg daily. However, there is evidence that 0.2mg orally daily is nearly just as effective at improving hair counts.^[4]https://pubmed.ncbi.nlm.nih.gov/10495375/ This dose also simultaneously reduces total drug exposure by 80%. For many people, this coincides with a reduction in perceived side effects.
• Try a topical formulation. Studies show that – when formulated properly – topical finasteride may reduce the risk of side effects by 30-90%. One 16-month study on 0.005% topical finasteride demonstrated significant hair improvements, no drug-associated side effects, and no impact on blood hormonal levels.^[5]https://www.tandfonline.com/doi/abs/10.3109/09546639709160517 This suggests that, at this dose, there is not enough leakage of finasteride from the scalp into the bloodstream to appreciably alter hormonal profiles – at least in the men and women in this study (though some people inside our membership have reported a different experience).
• Try intradermal delivery methods. Also known as mesotherapy, intradermal delivery methods inject finasteride into the scalp. But rather than use finasteride, consider using another 5-alpha reductase inhibitor: dutasteride. Evidence suggests that scalp injections of 0.01% x 1-2 mL of dutasteride – once every 1-3 months – do not appreciably alter serum hormones, nor do they result in any reported sexual side effects. They do, however, still lead to statistically significant hair improvements. Mesotherapy is more commonly done with dutasteride than finasteride, as dutasteride has a longer half-life (days-to-weeks versus 5-7 hours). This means fewer mesotherapy sessions are required to lower scalp tissue DHT (the hormone lowered by finasteride) for sustained periods.

For topical formulations and intradermal injections, testing personal blood levels of DHT before and during treatment can offer peace of mind. By quantifying the exact changes to serum DHT levels, it’s possible to see just how much topical finasteride (if any) is going systemic. In general, DHT fluctuations smaller than 20% are considered biologically insignificant. For more information on how to test serum DHT, look inside our ultimate guide to finasteride treatment.

So, consider the data first and foremost before giving up entirely on finasteride. It’s by no means guaranteed that finasteride lowers libido. Regardless, there are ways to leverage the power of this effective drug and simultaneously mitigate its risks.

What is Finasteride, and Which Finasteride is Best?

Finasteride is a drug approved by the FDA to treat benign prostate hyperplasia and androgenic alopecia. It is prescribed as a 1 mg daily tablet for men with androgenic alopecia. It is also prescribed in higher dosages for women suffering from female pattern hair loss. This ranges from 1.0-5.0 mg daily.

Finasteride is available in different formulations. The best option is determined on a patient-by-patient basis.

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What Formulations of Finasteride are Available?

There are two main finasteride formulations: oral and topical. Doctors typically prescribe oral finasteride, as it’s a time-tested formulation with a high success rate. Many telehealth providers have sprouted up in recent years, offering topical and oral versions of the drug. Topical finasteride has become increasingly popular as more studies confirm its efficacy and relative safety versus oral finasteride.

As concluded in one study:

Topical finasteride significantly improves hair count compared to placebo and is well tolerated. Its effect is similar to that of oral finasteride, but with markedly lower systemic exposure and less impact on serum DHT concentrations. ^[1]https://pubmed.ncbi.nlm.nih.gov/34634163/

Clinical studies have shown that oral and topical formulations improve hair parameters equivalently in target area hair counts.^[2]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9297965/ As such, many people looking to minimize their risk of side effects from finasteride often prefer the topical formulation, and they rationalize that decision by arguing that topical finasteride (1) is just as effective as oral finasteride, and (2) remains localized to the scalp, so it must not have any systemic effects elsewhere in the body.

In reality, both of these arguments are wrong.

1. While studies do show that topical finasteride is equivalent to oral finasteride in “target area hair counts”, hair count changes outside of these target zones have not yet been measured. Therefore, it is possible that topical finasteride may not protect against hair loss wherever it isn’t applied, whereas the oral formulation tends to provide global protection across the entire scalp. In fact, if topical finasteride does offer hair loss protection in non-applied scalp regions, the most likely reason is that the drug went systemic (i.e., entered into the bloodstream), traveled throughout the body, and redistributed to those non-applied areas. In that regard…
2. Topical finasteride can go systemic, depending on the dose. Several studies show that topical finasteride also lowers blood levels of DHT, particularly for daily doses totaling greater than 0.1 mg of finasteride exposure. While the amount of drug in circulation is still far less than that of oral finasteride, people trying topical finasteride should know this, and titrate their topical formulations accordingly. Just see this chart:

Finasteride 1mg Oral Tablets

As mentioned, finasteride is typically prescribed as a once-daily 1mg tablet. At 1mg daily, finasteride is sometimes branded as Propecia®. Using more than 1mg per day isn’t likely to improve results.^[3]https://pubmed.ncbi.nlm.nih.gov/10495375/

However, it may increase the risk of side effects. Nearly all clinical studies use 1mg, as it’s the gold standard for treating male pattern baldness. 5 mg finasteride is typically used to treat men diagnosed with benign prostatic hyperplasia (under the label Proscar®).

Oral Propecia® (i.e., 1mg daily of finasteride) is prescribed under its brand name and as a generic formulation through many telehealth companies. Generic versions of the drug typically deliver similar results, and often at a fraction of the cost.

Finasteride Topical Formulations

Finasteride topicals include gels, liquid solutions, and liquid sprays. Foams are available as well.

A previous post centered on the best topical finasteride dosage determined that finasteride has a highly-sensitive and dose-dependent response curve.

In other words, 0.01 mg of finasteride barely reduces any DHT, while 0.2 mg reduces almost as much DHT as 5 mg, a much larger dose.^[4]https://onlinelibrary.wiley.com/doi/10.1111/jdv.17738 1% topical formulations essentially guarantee systemic absorption.

Those aiming to avoid the side effects may want to consider a formula with lower percentages of the active drug.

Which Finasteride Is Best for Hair Loss?

It depends on two factors: (1) the presence of side effects, and (2) whether a patient has diffuse thinning or localized hair loss.

Side effects

When weighing the pros and cons of finasteride formulas, doctors often have patients start with oral finasteride. This is because oral finasteride has the strongest clinical evidence for treating male pattern hair loss, and it provides some degree of protection across all balding-prone areas.

If side effects occur on oral finasteride at 1 mg daily, doctors may consider lowering the dose to 0.2 mg daily to see if this reduces side effects. If issues persist, other options can be explored – such as topical formulations.

Under these circumstances, users may introduce topical finasteride at a 1-2 mL daily of 0.025% to 0.3% finasteride. If side effects persist, it may be necessary to lower that dose all the way to 0.005% x 2 mL daily, and start tracking serum DHT levels to measure – as a proxy – how much finasteride is actually going systemic (as these levels vary greatly depending on the person and any adjuvant treatments that might be influencing topical absorption – i.e., retinoic acid, microneedling, etc.).

Hair loss patterning

If someone wants to use topical finasteride, they should recognize that topical formulations of the drug are most appropriate for people who have localized hair loss (i.e., hair loss only at the temples and/or crown), rather than people with diffuse thinning (i.e., hair loss throughout the entire scalp).

This is because diffuse thinners have a larger area of the scalp to cover with a topical. That requires a higher amount of mL per application daily of topical finasteride to cover all zones. When holding constance the percentage dilution of topical finasteride, the more mL applied daily, the higher likelihood some of that additional finasteride will leak into the bloodstream and cause systemic effects – thereby defeating the whole effort of the topical in the first place.

For these reasons, diffuser thinners need to take extra care to titrate down their topical finasteride doses, or perhaps consider oral formulations of finasteride to maximize their scalp coverage and thereby improve their odds of long-term success.

For those who don’t experience any sexual side effects, long-term use of oral finasteride may be advisable, given its success rate. And for those who experience adverse systemic effects of oral finasteride, or those wary about potential issues with the oral formulation, topical finasteride may be the better option.

Finasteride and dutasteride are drugs that lower the hormone dihydrotestosterone (DHT), which is a hormone that is causally linked to both benign prostatic hyperplasia and male pattern hair loss. While both drugs tend to be effective hair loss treatments for men, they do come with a risk of side effects –most commonly sexual side effects and the growth of male breast tissue (gynecomastia).

These side effects are believed to occur because of finasteride and dutasteride’s inhibitory effects on 5-alpha reductase – an enzyme that helps convert free testosterone into dihydrotestosterone. By inhibiting this enzyme, finasteride and dutasteride are able to therapeutically lower DHT levels to improve the symptoms of an enlarged prostate and/or regrow hair. However, the inhibition of 5-alpha reductase can come with undesired side effects in 5-15% of men using these drugs – mainly due to the hormonal shifts that occur throughout the body when 5-alpha reductase activity is suppressed.

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Sexual Side Effects and Hair Loss Drugs

Based on clinical data (so far), there aren’t yet reliable blood tests to determine someone’s risk of sexual side effects from drugs like finasteride or dutasteride. Having said that, clinical studies show that men who have low levels of free testosterone and/or high levels of sex hormone binding globulin tend to be at the highest risk of “low libido”.^[1]https://pubmed.ncbi.nlm.nih.gov/25800960/

As such, some clinicians have argued (anecdotally) that patients reporting side effects from finasteride and dutasteride tend to already have hormonal imbalances associated with reduced libido prior to starting the drug. As such, these same clinicians sometimes suggest that by taking measures to (1) improve free testosterone, and/or (2) reduce sex hormone binding globulin – these men tend to see improvements to libido and, as a consequence, sport a higher tolerability for drugs like finasteride and dutasteride.

So, if you’re worried about sexual side effects from finasteride and dutasteride, there is at least some anecdotal and observational evidence suggesting that testing free testosterone and sex hormone binding globulin might help to predict your actual risk tolerance. With that said, it’s important to note that the data here remains limited.

Gynecomastia and Hair Loss Drugs

Gynecomastia is the growth of male breast tissue. It results from prolonged, elevated levels of the hormones prolactin and/or estrogen.

When it comes to the use of finasteride and dutasteride, blood tests can likely be used to determine someone’s risk of gynecomastia from both drugs.

Gynecomastia is estimated to affect between 0.25% to 1% of healthy people using 5-alpha reductase inhibitors, with 5-year retrospective studies in men with benign prostate hyperplasia suggesting an incidence of up to 3% to 5%. ^[2]https://pubmed.ncbi.nlm.nih.gov/23067029/

Interestingly, those who start finasteride and/or dutasteride while already having elevated levels of prolactin and estrogen might be at a higher risk of developing gynecomastia. This is because drugs like finasteride and dutasteride can raise blood levels of both testosterone and/or estrogen by 10-20%, depending on the dose.^[3]https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/020788s020s021s023lbl.pdf^[4]https://journals.sagepub.com/doi/abs/10.1177/2051415820926301 Consequently, as blood levels of estrogen and/or prolactin rise, these hormones can stimulate the growth of ductal tissue and alveolar differentiation – both of which relate to the growth of male breast tissue.^[5]https://www.ncbi.nlm.nih.gov/books/NBK279105/

So, for those starting the drug with borderline-high estrogen, the additional lift in estrogen levels may put someone in the “danger zone” for gynecomastia.

Blood Tests for Finasteride and Dutasteride

For peace of mind, people can always order blood tests for prolactin and estrogen prior to starting finasteride or dutasteride. Additional tests can be performed further down the line.

If levels are within range, the risk of gynecomastia is likely much lower. This can be done with a primary care physician. Those based in the U.S. (and other countries that offer direct-to-consumer lab testing), can order tests through the links below.

• Direct-To-Consumer Lab Test: Prolactin (U.S. only)^[7]truehealthlabs.com/product/prolactin
• Direct-To-Consumer Lab Test: Estrogen (U.S. only)^[8]truehealthlabs.com/product/estradiol-e2
• Finasteride: Ultimate Guide (Member’s Only)

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What a Blood Test for Finasteride Can Do

While it’s up for debate if blood tests can actually predict someone’s risk of sexual side effects from finasteride or dutasteride, there is evidence that estrogen and prolactin levels pre-hair loss drugs might give some insights into the risk of developing gynecomastia. The totality of evidence suggests that finasteride and dutasteride may raise estrogen levels by 10-20%. Therefore, if your pre-finasteride levels of estrogen and/or prolactin are within 10-20% of the upper limit, it’s probably best to find ways to lower these levels before committing to the drug.

Diet, lifestyle, and environmental changes are often enough to normalize these hormones in many men.

What about Blood Tests to Predict Hair Regrowth from Finasteride?

The best predictor of hair regrowth from finasteride comes not from a blood test, but from an accurate hair loss diagnosis. After all, two-year clinical studies show that in otherwise healthy men with androgenic alopecia that presents in its standard horseshoe pattern, response rates for finasteride tend to hover around 80-90%.^[9]https://www.sciencedirect.com/science/article/pii/S0022202X15529357

Recently, marketers have begun pushing genetic testing to determine someone’s response rate to finasteride and dutasteride. Preliminary data from poorly designed clinical studies suggests that perhaps there are some genes associated with higher-magnitude responses from both drugs, and also a better success rate. For instance, one study suggested that genetic “CAG repeat score” might help determine the response rate to finasteride, and that this data could be collected through blood draws.^[10]https://pubmed.ncbi.nlm.nih.gov/31949455/

But again, the evidence here is limited and preliminary. Given the overwhelmingly high odds of a response to finasteride overall, we tend to place more weight on an accurate diagnosis than on genetic testings for either drug.

Finasteride Side Effects

Finasteride is the most powerful, well-studied, FDA-approved drug for androgenic alopecia (AGA). It stops AGA progression in 80-90% of men and, on average, leads to a 10% increase in hair count over two years. For men wanting a hands-off approach to hair maintenance, finasteride is often an excellent option.

That said, finasteride isn’t for everyone. While its risk of side effects are often overstated online, the drug appears to reduce libido in a certain percentage of men and may induce gynecomastia. The drug can also temporarily lower sperm counts, which might make conception more difficult during its first six months of use. In some men, the use of finasteride appears to increase anxiety and/or depression. 

The true incidence and magnitude of these reports are hard to discern. Depending on the study we cite and the questionnaire design, these effects can range from 1% to 40%. Whether or not one should worry about finasteride side effects may depend on their current hormonal profile and mental health. Keep reading to learn more.

Interested in Topical Finasteride?

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

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

Gynecomastia

Gynecomastia is the growth of male breast tissue. It results from elevated hormones such as prolactin and estrogen. While gynecomastia is estimated to only affect between 0.25-1.00% of people on 5-alpha reductase inhibitors (such as finasteride), those who start the drug with already elevated levels of prolactin and estrogen are likely at a higher risk of its development. 

Drugs like finasteride can raise blood levels of both testosterone and estrogen by 10-30%, depending on the dose. So, for those starting the drug with borderline-high estrogen, the additional lift in estrogen levels may put someone at greater risk of gynecomastia.

Sexual Side Effects

Because it lowers DHT levels (a hormone that helps maintain male sex characteristics), some studies have shown that a percentage of finasteride users report sexual side effects ranging from decreased sex drive to reduced semen volume to erectile dysfunction. Studies vary widely, but incidents could be as low as 1-2% of users.

Female users should be aware that Finasteride can potentially mutate and/or inhibit the development of male fetus genitalia.^[1]dailymed.nlm.nih.gov/dailymed/lookup.cfm As such, pregnant women are neither prescribed finasteride nor advised to even handle the medication. 

Cognitive Side Effects

On hair loss forums, some men taking finasteride have complained of changes to cognition, specifically, a feeling of brain fog since starting therapy. To date, this hasn’t been reported to significant degrees in clinical studies. This may be because even if the effects do exist, it’s likely a subtle, gradual side effect that many may not attribute to the drug. 

Animal models have demonstrated that finasteride can indeed change brain chemistry, especially after transitioning off of the drug. But it’s important to note that animals in those studies take dosages of finasteride thousands of times greater than what is prescribed to humans.

In any case, it’s not unreasonable that those with depression, anxiety, and/or bipolar disorder should proceed with caution and speak with their doctor to closely monitor the effects of finasteride use.

How To Reduce Side Effects Of Finasteride

Regardless of the specific side effect that’s being targeted to reduce, the strategies are all similar: find ways to (1) reduce daily drug exposure, (2) localize the drug’s effects to the scalp, and (3) do lab tests to determine personal risk for certain side effects like gynecomastia. These strategies are outlined in detail below:

Limit Daily Drug Exposure

As a hair loss drug, finasteride is typically prescribed orally at 1mg daily. Having said that, there’s evidence that 0.2mg daily is nearly just as effective at improving hair counts while simultaneously reducing total drug exposure by 80%. For many people, this coincides with a reduction in perceived side effects.

If side effects, or anticipatory anxiety, are a concern, try lowering the dose of the drug from 1mg daily to 0.2mg daily. After all, small clinical studies have demonstrated that doses as low as 0.2mg daily still improve hair counts, and may also confer a slightly smaller magnitude and/or severity of side effects (at least anecdotally).^[2]https://pubmed.ncbi.nlm.nih.gov/10495375/

Unfortunately, finasteride is a hair loss drug that must be continued indefinitely for its effectiveness to remain. When finasteride treatment is stopped, men typically lose what hair regrowth they gained within 3-12 months. For these reasons, it’s not advised to drop below doses equating to 0.2mg daily – as efficacy may rapidly diminish below this threshold.

If finasteride side effects don’t go away with reduced usage, most users report any lingering side effects go away after discontinuing the drug within 2-3 weeks, and for some, up to a few months. If problems persist beyond that, it’s important to contact your prescribing physician.

Localize Finasteride’s Effects to the Scalp

There are two primary ways to localize finasteride’s effects to the scalp. These methods minimize the amount of the drug that circulates throughout the bloodstream, thus minimizing the side effects of finasteride. Both entail switching from an oral to topical formula.

Try a topical formulation

Studies show that – when formulated properly – topical finasteride may reduce the risk of side effects by 30-90%. One 16-month study on 0.005% topical finasteride demonstrated significant hair improvements, no drug-associated side effects, and no impact on blood hormonal levels.^[3]https://dx.doi.org/10.3109%2F09546639709160517 This suggests that any absorption of the drug beyond the scalp was metabolized quickly enough to not impact serum DHT levels.

Other studies have demonstrated that higher doses of topical finasteride also confer benefit, and at smaller reductions of serum DHT (i.e., a proxy for systemic absorption) and perhaps side effects, too.^[4]https://onlinelibrary.wiley.com/doi/full/10.1111/jdv.17738 Having said that, if minimizing side effects are a top priority, we still recommend starting with the minimum viable dose of topical finasteride – 0.005% x 2 mL daily – and working your way up from there.

Try intradermal delivery methods (dutasteride)

Also known as mesotherapy, intradermal delivery methods inject finasteride into the scalp. While there aren’t yet clinical studies of mesotherapy finasteride in reputable journals, there are clinical studies of mesotherapy dutasteride – a drug that is more powerful at reducing DHT levels versus finasteride and that also has a longer half-life (which makes it a better candidate for less-frequent injections into the scalp – since the drug will stay active for longer).

A small number of clinical studies suggest that scalp injections of ~0.01% x 1-2 mL of dutasteride, once every 1-3 months, do not appreciably alter serum hormones, nor do they result in any reported cognitive or sexual side effects. They do, however, lead to statistically significant hair improvements.

Determine Your Risk for Finasteride Side Effects

Determining personal risk ahead of time, and getting a baseline measure of hormonal health, can help people decide if finasteride is right for them. It can also help people keep track of how the drug is influencing their serum hormones.

Testing for Sexual Side Effect Risk

There aren’t yet clinical studies demonstrating the predictability of finasteride side effects related to lowered libido or sexual dysfunction. There are, however, clinical studies suggesting men who are experiencing reduced libidos tend to also have low levels of free testosterone and/or high levels of sex hormone binding globulin.

For these reasons, some clinicians recommend getting these hormones tested prior to starting finasteride. While finasteride isn’t known to have a major influence over these hormones, borderline-abnormal tests may make someone more likely to report these problems, irrespective of whether they’re using hair loss drugs.

Testing for Gynecomastia Risk

For peace of mind, blood tests for prolactin and estrogen can be ordered prior to starting finasteride. Clinical studies do show that finasteride and dutasteride can slightly increase levels of estrogen, and that a rise in estrogen and/or prolactin can be pathogenically linked to the development of gynecomastia, also known as male breast development.^[5]https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/020788s020s021s023lbl.pdf^[6]https://journals.sagepub.com/doi/abs/10.1177/2051415820926301^[7]https://www.ncbi.nlm.nih.gov/books/NBK279105/

If you’re worried about this side effect, test your estrogen and prolactin levels. If they’re within 10-20% of the upper limit for normal, then finasteride or dutasteride use may put you “over the edge” and into that risk category of gynecomastia. Under these circumstances, consider dietary, lifestyle, and/or environmental interventions to lower levels of these into a normal range prior to starting finasteride, and rechecking these hormones regularly or if breast tenderness begins to develop.

Also keep in mind that blood tests for hormones are just proxies for what might be occurring elsewhere in the body. Therefore, it’s entirely possible for serum blood tests to mislead us into thinking we have “normal” levels of hormones, when our tissue hormonal profiles might be out-of-range. The inverse is also true: out-of-range blood hormones don’t always signify out-of-range tissue hormones. So, treat any laboratory test as preliminary, and recognize the science supporting these tests – at least for their predictability of finasteride side effects – is still in its infancy. 

Anyone interested in doing these lab tests can do so with the help of their primary care physician. Or, those based in the U.S. (or any other country that offers direct-to-consumer lab testing) may be able to order tests through the links below.

For more information, see these resources (no affiliate links):

• Direct-To-Consumer Lab Test: Prolactin (U.S. only) ^[8]truehealthlabs.com/product/prolactin
• Direct-To-Consumer Lab Test: Estrogen (U.S. only) ^[9]truehealthlabs.com/product/estradiol-e2

Can We Localize Finasteride Entirely To The Scalp?

Topical finasteride can still go systemic. Having said that, clinical studies also show that daily doses of topical finasteride as low as 0.005% x 2 mL can still produce positive hair parameter changes over 16 months, and without impacting serum DHT levels (a proxy for systemic circulation of the drug).

For those worried about the sexual side effects of finasteride, this formulation of topical finasteride might be most appropriate. However, if you go down this route, you also may want to consider periodically testing serum DHT levels – as members inside our membership community have found that even at these ultra-low dilutions of finasteride, serum DHT tests can still decline by more than 25%. 

Changes to serum DHT levels can help people understand just how much topical finasteride (if any) is going systemic. In general, DHT fluctuations smaller than 20% are considered biologically insignificant.

Directions for how to do this can be found inside our comprehensive finasteride guides, available only to members. 

So, consider these options (and the data) before giving up entirely on finasteride. There are many ways to leverage its power, mitigate its risks, and perhaps take your hair regrowth to a new level.

Topical Finasteride

Finasteride is a hair loss drug for treatment of androgenic alopecia. It inhibits the 5-alpha reductase type II enzyme that converts testosterone into dihydrotestosterone, or DHT.

Topical finasteride formulations (think: solution, spray, or gel) are growing in popularity because of their localized approach. Oral finasteride reduces DHT everywhere in the body. Topical finasteride reduces DHT in the area that it is applied while minimizing systemic absorption. That is, if you apply it correctly. The question of how to apply topical finasteride for the greatest benefit and the least systemic absorption has no single, easy answer.

Interested in Topical Finasteride?

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Applying Topical Finasteride to the Scalp

Strategies for applying topical finasteride depend on its formulation (spray, solution, serum, or gel). We’ll review those first, then explain how long topical finasteride needs to stay on the scalp in order to absorb and have an effect (hint: it depends on the dosage and carrier agent).

How to Apply Topical Finasteride Spray

Many hair loss sufferers opt for topical finasteride spray. These sprays are often used to disperse the drug over wide surface areas of scalp skin, and are most appropriate for people with (1) thinning over widespread areas who also (2) are keeping their hair very short so that the scalp skin is easily accessible.

If you have diffuse thinning and longer hair, sprays might not be right for you. This is because too much of the topical finasteride will end up on the hair (where it does nothing) rather than the scalp (where hair grows from).

Users are advised to hold the spray bottle 2-3 inches from the scalp and apply the prescribed amount on the crown, top, and front of their heads. The hands can then be used to rub in any liquid blocked by existing hairs. This will ensure that a considerable amount of the formula has reached the scalp, particularly in problem areas.

Some users prefer to spray the formula into their palms and apply it manually with their fingertips. As with other formulas, parting sections of hair may make it easier to apply.

How to Apply Topical Finasteride Solution

Topical finasteride is also prescribed in the form of a liquid solution. These variations may include minoxidil as a combination therapy. Such formulas typically include a dropper for easy application. To apply the solution, part the hair in sections, apply a few drops along the part, then rub the solution around the scalp skin with the fingertips. Additional drops can then be applied to key problem areas (crown, top, and both sides of the front).

Alternatively, the prescribed amount can be dispensed into the hand and applied manually.

How to Apply Topical Finasteride Gel

Gel formulations are often made of bases of silica and/or liposomes. They’re very popular, as they are easy to apply. For best results, users can start with a few pumps of the gel, applying with their hands to provide even coverage across each problem area. The gel should gently be massaged into the scalp for 30 seconds or more.

No matter the treatment form, it’s only necessary to cover the areas affected by hair loss. Users should always follow their doctor’s recommendations and consult the directions included in their formula.

Any excess formula should immediately be washed off of hands and other areas of the body.

How Long Should Topical Finasteride be left on Scalp?

How long to let topical finasteride sit on your scalp depends on several factors, including:

1. The dilution (the % finasteride in your topical formulation)
2. The daily mL applied (alongside % dilution, this will determine your daily total exposure volume of finasteride in mg)
3. The carrier ingredients in your topical (this will determine how much – and how quickly – topical finasteride will move from outside of the scalp into the dermis, where it can actually elicit an effect on hair follicles)

To understand more of this process, we also need to understand the stages of absorption when applying any drug to our scalp skin:

• Stage #1: the drug sits on the epidermis (i.e., 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.

An in vitro study measured percutaneous absorption of topical finasteride across a variety of different formulations: ethosomes, ethanol, liposomes, and aqueous (water). ^[1]ncbi.nlm.nih.gov/pmc/articles/PMC2977015

This chart shows the percent of topical finasteride that percutaneously absorbs (enters the dermis) over a 24-hour period:

There are three big takeaways from this chart:

1. The longer topical finasteride is left on the scalp, the more drug will be absorbed percutaneously.
2. Across carrier ingredients, absorption rates appear to be linear. At 10 hours of contact, 2-13 micrograms of finasteride are absorbed into the skin, depending on the carrier. At 20 hours, those numbers double to 4-26 micrograms.
3. When it comes to finasteride skin penetration, carriers rank from best to worst as ethosomes > hydroethanol > lipsomes > water.

Finasteride Absorption Rates

Leaving finasteride on the scalp for 10 hours allows for 5 micrograms per square centimeter of percutaneous absorption across most carrier agents. Is this enough finasteride to therapeutically lower scalp DHT levels? More importantly, is it enough to regrow hair?

There is not a clinical study that attempts to answer this. However, there is some surrogate data to help us approximate the answer.

A certain percentage of topical finasteride will absorb into the dermis. The bloodstream will absorb some of this later. Time-dependent DHT reductions in the bloodstream can be used to “ballpark” how much DHT is likely also being reduced in the scalp. This is because there is more topical finasteride that percutaneously absorbs than systemically absorbs. 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.

This figure from a 2014 study measures the effects of one versus two applications of 1 mL of 0.25% topical finasteride on serum DHT levels. ^[2]https://pubmed.ncbi.nlm.nih.gov/25074865/

Optimal Amount of Time

Six hours after applying 1 mL or 2 mL applications of 0.25% topical finasteride (i.e., 2.275-4.550 mg of finasteride), serum DHT reductions flatline. By the 6-hour mark, the 2ml application group experienced roughly the same serum DHT reductions as would be expected from a 1mg oral dose of finasteride.

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

Topical finasteride applications of 2.275 mg or higher (with a hydroxypropyl chitosan delivery vehicle) achieve systemic reductions in DHT. Furthermore, the larger dose of topical finasteride reduces systemic DHT levels on par with oral finasteride.

Serum DHT reductions are only achieved after scalp DHT reductions occur. Because of this, the conclusion can be drawn that 6-12 hours after applying topical finasteride, there’s likely enough percutaneous absorption to therapeutically lower scalp DHT levels for hair regrowth. However, this time window depends on a number of factors, including:

• Finasteride dilution (%). After all, the percent of finasteride, in part, determines your total daily exposure of finasteride. Remember that finasteride’s absorption is linear, so the higher the dilution, the more finasteride will absorb.
• The daily mL applied. Along with the percentage dilution of finasteride, the mL of topical applied will determine our total daily exposure of finasteride placed on the scalp.
• The carrier ingredients used. As we learned in the previous study, water-based carriers perform the worst at carrying finasteride into the skin, while ethosomes and water-alcohol mixes perform the best.

The next logical question becomes, just how low of a dilution of finasteride can you apply to evoke hair growth outcomes, while still potentially preserving serum DHT levels to the best of your ability? Interestingly, there seems to be a “sweet spot” for this at ~0.1 mg daily of topical finasteride mixed with alcohol and propylene glycol as carriers.

A 1997 study corroborates this. The study suggests that 2 mL daily of 0.005% topical finasteride (i.e., 0.0912 mg of finasteride exposure) improved hair parameters for men with AGA. This was achieved without affecting serum DHT levels – even after 16 months of treatment. ^[3]https://www.tandfonline.com/doi/abs/10.3109/09546639709160517

For Most Topical Finasteride Formulations, 6-12 Hours is Long Enough

Most big-brand topical finasteride companies are:

• Selling dilutions mixed with alcohol, propylene glycol, or glycerin
• Selling dilutions of 0.1% to 0.3% finasteride
• Advising patients to apply at least 1-2 mL daily

For most users, this will equate to 1 mg to 6 mg of topical finasteride exposure daily – which is more than 100x the minimum viable dose of topical finasteride. At these dosage ranges, the evidence suggests that topical finasteride will only need  6-12 hours on the scalp to therapeutically lower scalp DHT levels and start encouraging hair growth.

Topical finasteride users should use this time window to their advantage! But they should also keep in mind that, at most big-brand dose ranges, they’re exposing themselves to just as much (if not more) finasteride than the oral formulations. So they might be overpaying for topical finasteride in hopes of “localizing” its effects, only to also have just as much – if not more – of that drug going systemic.

To get the true benefits of localization, users will likely need to drop their dose as low as 0.005% x 2 mL daily, and periodically track serum DHT levels to ensure systemic effects are minimal.

The instructions on the packaging aren’t always as precise as the research. Best to trust the science when it comes to how to apply topical finasteride for maximum effectiveness, and minimal side effects.

According to 2021 estimates, over 20% of people in the U.S. use antidepressants or antianxiety medications. Within this group of medications, hair loss is sometimes listed as a known side effect. 

Mostly, these drugs cause temporary hair loss that goes away after a period of acclimation or after the drug is discontinued. But for the 1 in 5 people who use these drugs to support mental wellbeing, there’s a very real fear that mood stabilization might only be available at the expense of their hair.

The good news is that hair loss from anxiety medications is relatively uncommon. And while it can occur, there are ways to mitigate the risk of hair fall.

This article takes a scientific look at the relationship between the most commonly prescribed psychotropic drugs and hair loss, revealing science-based recommendations for those who are affected by hair loss and worried that their antidepressants are to blame.

• What type of hair loss is associated with psych meds?
• What evidence shows a link between psychopharmaceuticals and hair loss?
• Is there indeed a cause and effect relationship? 
• What does this mean for those prescribed to these medications?

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Types of Drug-Induced Hair Loss

Drug-induced alopecia typically falls into two main categories: telogen effluvium and anagen effluvium. These names refer to the stage in the hair cycle where growth is interrupted.^[1]https://link.springer.com/article/10.2165/00002018-199410040-00005

Telogen Effluvium

Telogen effluvium is the most common type of drug-induced hair loss. With this condition, hair follicles are prematurely triggered to enter their resting (telogen) phase, which induces early shedding. The condition typically becomes noticeable within 2-4 months of beginning treatment. 

Anagen Effluvium

Anagen effluvium occurs during hair’s growth (anagen) phase. Hair cells that should be rapidly dividing are triggered to abruptly stop. This type of drug-related hair loss occurs within days or weeks of treatment and is not limited to the scalp. It is most commonly associated with chemotherapy drugs. 

Medication-induced alopecia, in particular telogen effluvium, is a known side effect of some psychopharmaceuticals. Hair loss is typically temporary and may resolve on its own, or with a reduction in dosage. Discontinuation of these drugs nearly always leads to hair regrowth.^[2]https://pubmed.ncbi.nlm.nih.gov/10798824/

What About Androgenic Alopecia (AGA)?

Psychopharmaceuticals do not cause androgenic alopecia (male pattern baldness), but may temporarily accelerate the condition. If several hair follicles in AGA-prone regions suddenly enter the telogen phase, hair follicle miniaturization can increase, speeding the progression of AGA. 

Psychotropic Medications and Hair Loss: The Research

It’s important to note that just because hair loss is listed as a potential side effect of certain medications does not mean it will happen to everyone. But, it can still happen. What’s most important is the percent of people reporting hair loss in a clinical trial for any of these drugs.

Among the class of drugs referred to as psychopharmaceuticals, hair loss is most frequently associated with long-term use of lithium and valproic acid. 

As many as 19% of lithium users and 12% of valproic acid users report the unwanted side effect.^[3]https://pubmed.ncbi.nlm.nih.gov/10798824/ For most other drugs, risk is much lower, and possibly as low as 0.01%.

To learn more about the actual connection between antidepressants, anti-anxiety medications, mood stabilizers and hair loss, the Perfect Hair Health team combed through hundreds of case studies. 

The Process

First, the team looked at the most commonly prescribed medications and then ran those drug names through a research database to pull up any and all studies that mentioned hair loss. Below is an overview of what was found. 

If a drug is not the list, it’s either because no reports of hair loss were not found or commonly prescribed. Others were simply not worth mentioning for various reasons. To jump to a particular drug, use the links below.

Antidepressants

• SSRIs
  • Escitalopram (Lexapro)
  • Fluoxetine (Prozac)
  • Paroxetine (Paxil)
  • Sertraline (Zoloft)

• Atypical Antidepressants
  • Bupropion (Wellbutrin)

• Atypical Antipsychotics
  • Olanzapine (Zyprexa)
  • Quetiapine (Seroquel)

Anti-Anxiety Medications

• Benzodiazepines
  • Clonazepam (Klonopin)

• Buspirone
• Antimantic Agents
  • Lithium
  • Valproic Acid

Evaluation Of Evidence Quality

Of the several studies cited below, most consist of case reports that reference just a single individual. What’s more, these case reports often make it to publication precisely because of their uniqueness. In these reports, researchers often make reference to ‘the first known case’ or ‘the only known case.’ 

Case studies rank relatively low on the hierarchy of evidence, as they are very anecdotal, and not supported by double-blind research, for example. This makes it hard to know the true incidence or prevalence of hair loss from many of these drugs. 

Antidepressants and Hair Loss

Antidepressants are of several different classes, namely selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), MAOIs, and atypical medications. 

SSRIs and Hair Loss

Selective serotonin reuptake inhibitors (SSRIs) are among the most commonly prescribed antidepressants and are sometimes used to treat anxiety disorders. Of these, hair loss is associated with the following medications:

• escitalopram (Lexapro)
• fluoxetine (Prozac)
• paroxetine (Paxil)
• sertraline (Zoloft)

The team did not find any studies linking two other common SSRIs, protriptyline (Vivactil) and amitriptyline (Elavil) with hair loss. Take a closer look at what was found.

Escitalopram (Lexapro)

2021 Case Study: 

A male patient diagnosed with major depressive disorder experienced hair loss with escitalopram. The patient discontinued escitalopram when he could no longer tolerate the hair loss. The hair loss stopped within one month.^[4]https://www.psychiatria-danubina.com/UserDocsImages/pdf/dnb_vol33_no2/dnb_vol33_no2_187.pdf

2020 Case Report: 

A female patient on 5mg escitalopram reported minor hair loss. After her dose was increased to 10mg, hair loss became ‘significant.’ After quitting the drug due to intolerable hair loss her symptoms ‘dramatically’ resolved within one week.^[5]https://www.psychiatrist.com/pcc/depression/escitalopram-induced-hair-loss/

2016 Case Study:

This case study is unusual because the female patient presented with eyelash loss 12 weeks after beginning treatment with escitalopram. Her eyelashes returned to near normal 5 weeks after she stopped taking the medication. 

While SSRIs are known to cause alopecia, this is the first reported case of eyelash loss. Researchers noted the timing of the patient’s presentation was consistent with the growth cycle of eyelashes, suggesting the mechanism of loss was interruption of the hair growth cycle.^[6]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5035805/

2011 Case Study:

Woman suffering from major depressive disorder noticed hair loss 3 weeks after beginning escitalopram. She discontinued the drug due to intolerable hair loss. Two weeks later, the hair loss stopped. 

Several months later she tried the drug again as her depressive symptoms had returned. After 2 weeks? Her hair loss returned.^[7]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3219523/  

Fluoxetine (Prozac)

2021 Case Study:

Six weeks after beginning fluoxetine, a male patient reported hair loss in the frontal region of the skull. His complaints ended after he stopped taking the drug. This case appears to be the first evidence of fluoxetine-related hair loss in men.^[8]https://pubmed.ncbi.nlm.nih.gov/34355374/ 

2019 Case Study:

Six weeks after beginning fluoxetine, a female patient reported hair loss in the frontal region of the skull.^[9]https://pubmed.ncbi.nlm.nih.gov/31599441/

2018 Case Report: 

Female patient notices significant hair loss 2 weeks after beginning fluoxetine. By 18 months, she had lost all her scalp and body hair. Researchers are aware of just one other similar case, and suggest there may be a wider spectrum of fluoxetine-related hair loss than previously known.^[10]https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/article/hair-loss-associated-with-fluoxetine/D2A55E09DDCF393399C14DB9289BAADE

2004 Case Study:

Female patient reports slight hair loss 3 months after beginning fluoxetine 20mg treatment. Reducing the drug to 10mg had no effect on her hair loss. After 1 year she stopped treatment due to intolerable hair loss on the scalp and body. 4 weeks later, her hair returned to normal thickness.^[11]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC514846/

1992 Drug Trial:

A group of 15 young adults, ages 16-24, trialed fluoxetine for the treatment of their depression. Researchers noted that the side effect of alopecia appeared more commonly than in adult studies.^[12]https://pubmed.ncbi.nlm.nih.gov/19630647/  

Paroxetine (Paxil)

2021 Case Report:

Male with social anxiety disorder reports hair loss after beginning treatment with paroxetine. The hair loss stopped after discontinuing the drug, then recurred when treatment with paroxetine began again.^[13]https://pubmed.ncbi.nlm.nih.gov/34181746/

2006 Case Study:

Over 60% of patients with alopecia areata (AA) have a psychiatric comorbidity. Researchers hypothesize that treating this depression may have a positive effect on hair growth. In this case study, a female patient had complete hair regrowth 7 weeks after beginning paroxetine treatment. One month after discontinuing the drug, her symptoms of AA had returned.^[14]https://sci-hub.se/https://pubmed.ncbi.nlm.nih.gov/16922952/

2001 Double-Blind Randomized, Placebo-Controlled Trial: 

A group of 13 patients presenting with AA and a psychiatric comorbidity were studied to see if treatment with SSRIs could lead to regrowth of hair. Researchers observed the complete regrowth of hair in two patients treated with paroxetine, while four showed partial regrowth. Meanwhile, only one patient from the placebo group had similar regrowth.^[15]https://pubmed.ncbi.nlm.nih.gov/11737460/

2000 Case Report:

‘Massive’ hair loss was reported in a woman being treated with paroxetine, which improved soon after she stopped taking the drug.^[16]https://pubmed.ncbi.nlm.nih.gov/10883182/

1999 Case Report:

A female complained of ‘moderate’ hair loss after beginning paroxetine treatment. The hair loss stopped after discontinuing the drug, and began again when the drug was reintroduced.^[17]https://pubmed.ncbi.nlm.nih.gov/10442258/

Sertraline (Zoloft)

2015 Case Study:

A male patient reports hair loss 2 weeks after beginning sertraline treatment. His hair loss improved after he stopped taking the drug.^[18]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4589582/

2008 Case Study:

A woman complained of hair loss during sertraline treatment. This case is unique because she had previously been treated with fluoxetine, but reported no hair loss during that treatment.^[19]https://pubmed.ncbi.nlm.nih.gov/18664165/

2006 Literature Review:

Researchers reviewed all reports of SSRI-induced hair loss in the national Swedish database and the database for the World Health Organization. Reports of sertraline-induced hair loss were nearly double those for citalopram, although still considered a ‘rare’ side-effect.^[20]https://pubmed.ncbi.nlm.nih.gov/16783834/

2005 Case Study:

A 14 year old boy reports hair loss after 5 years of sertraline treatment. The drug was gradually discontinued and the hair loss stopped.^[21]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3000200/

Atypical Antidepressants

Bupropion (Wellbutrin)

Bupropion is an atypical antidepressant. It is not an SSRI or an SNRI, but an NDRI. It’s used not only to treat depression, but sometimes prescribed to help with smoking cessation.

2018 Research:

In a study that followed over 1 million patients, researchers tracked exclusive users of antidepressants to better understand hair loss risk. They found that compared with bupropion, all other antidepressants had a lower risk of hair loss. Fluoxetine and paroxetine ranked as being lowest risk, with the highest level of confidence. 

The researchers concluded that of all the SSRIs and SNRIs, bupropion has the highest risk of hair loss, while paroxetine has the lowest.^[22]https://pubmed.ncbi.nlm.nih.gov/28763345/

Atypical Antipsychotics

Olanzapine and quetiapine are classified as atypical antipsychotics. Both are used in the treatment of bipolar disorder, while quetiapine is also sometimes used to treat major depressive disorder.

Olanzapine (Zyprexa)

2002 Case Report:

After increasing her daily dose of olanzapine from 5mg to 15mg daily, a woman reports increasing hair loss. Hair loss discontinued after switching from olanzapine to risperidone. Researchers report that this is the first known case of olanzapine-induced hair loss, and note the manufacturer, Eli Lily Canada, estimates hair loss occurs among just 0.01% of users.^[23]https://sci-hub.se/https://pubmed.ncbi.nlm.nih.gov/12500769/

Quetiapine (Seroquel)

2007 Literature Review:

Researchers reviewed all case reports of alopecia following quetiapine treatment reported to the New Zealand Intensive Medicines Monitoring Programme and the World Health Organization. They found 17 cases total, some of which support a causal relationship between quetiapine and hair loss. Researchers note that while hair loss has previously been associated with both olanzapine and risperidone, it has not yet been described with quetiapine.^[24]https://pubmed.ncbi.nlm.nih.gov/17293712/

Anti-Anxiety Medications and Hair Loss

Benzodiazepines and Hair Loss

Benzodiazepines are classified as depressants and can help patients who struggle with anxiety. Of this class of drugs, only clonazepam seems to be associated with hair loss. There were no studies connecting alprazolam (Xanax), diazepam (Valium) or lorazepam (Ativan) with hair loss. 

Clonazepam (Klonopin)

2009 Case Study:

A woman complains of hair loss one week after beginning treatment with clonazepam. The hair loss stopped when she stopped taking the drug. Researchers note they reviewed the literature and found only one other case of hair loss associated with clonazepam. Also noted, she had been taking escitalopram (which has a more well-documented association with hair loss) prior to her hair shedding and continued with this drug even as her hair grew back.^[25]https://pubmed.ncbi.nlm.nih.gov/19471188/

Buspirone

Busiprone is categorized as an ​​anxiolytic, and is used to treat both short-term and chronic anxiety. 

2013 Case Report:

A woman being treated with buspirone and sertraline reports significant hair loss. Her treatment team discontinued buspirone, but not sertraline (which is also associated with hair loss). The patient reported her hair loss stopped 3-5 days later, although researchers noted they couldn’t confirm.^[26]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579479/

Antimanic Agents

Antimanic agents are mood stabilizers. They are used in the treatment of bipolar disorders and can calm those in states of mania or extreme anxiety. Of this class of drugs, lithium and valproic acid are most frequently associated with hair loss. 

Lithium 

2013 Literature Review:

A meta analysis on the side effects of lithium finds no statistically significant increase in risk of hair loss with lithium treatment. Researchers mention that lithium suppresses the thyroid, which could be related to reports of hair loss.^[27]https://pubmed.ncbi.nlm.nih.gov/23525591/

2012 Literature Review:

A review of 385 abstracts were screened for reports of lithium toxicity, including lithium-induced alopecia. Researchers found no significant risk of alopecia associated with lithium.^[28]https://pubmed.ncbi.nlm.nih.gov/22265699/

1994 Case Study:

A woman reports hair loss after beginning lithium treatment. 2 months after discontinuing treatment, her alopecia resolved. Researchers note this side effect is rare.^[29]https://pubmed.ncbi.nlm.nih.gov/7995585/

1988 Case Study:

A patient reports total hair loss after 2 months of lithium treatment. Researchers discuss a possible connection between the drug and alopecia totalis.^[30]https://pubmed.ncbi.nlm.nih.gov/3126095/ 

1984 Literature Review:

Researchers review all cases since 1970, when lithium-related hair loss was first reported. They suggest patients experiencing hair loss after lithium treatment be checked for hypothyroidism, because lithium ions may concentrate in the thyroid, disrupting normal processes in this area.^[31]https://pubmed.ncbi.nlm.nih.gov/6519870/

1983 Case Report:

Of 100 patients on lithium therapy, 12 report hair loss. 1 patient was diagnosed with hypothyroidism, others experienced hair regrowth after discontinuing treatment.^[32]https://pubmed.ncbi.nlm.nih.gov/6838778/

1983 Case Study:

Researchers present 2 cases of hair loss attributed to lithium therapy. They recommend thyroid tests to exclude hypothyroidism as the cause of hair loss.^[33]https://pubmed.ncbi.nlm.nih.gov/6404546/

1982 Case Report:

Researchers study 7 cases of hair loss associated with lithium. They mention other findings that for those with scalp psoriasis, lithium can aggravate this condition. They report findings consistent with telogen effluvium and conclude lithium can cause increased hair shedding. ^[34]https://pubmed.ncbi.nlm.nih.gov/6809028/

Valproate/Valproic Acid

2018 Case Study:

A review of over 400,000 patients being treated with psychotropic drugs in German-speaking countries found that Valproic acid was related to the highest risk of hair loss. That said, researchers found just 43 cases, a number distinctly lower than expected.^[35]https://pubmed.ncbi.nlm.nih.gov/30193142/

2018 Literature Review:

A review of literature finds Valproate-induced hair loss is diffused, nonscarring, and dose-related. The drug may also cause graying and changes to hair texture. Researchers note that topical valproic acid may help hair regeneration and suggest further study into the difference between oral and topical administration as they relate to changes in hair growth.^[36]https://pubmed.ncbi.nlm.nih.gov/30386073/

2017 Research:

Hair loss is a well-known side effect of valproic acid. It leads to telogen effluvium and appears to be dose-dependent, meaning hair loss increases with increased dosage. Paradoxically, valproic acid can be applied topically to help regrow hair. Researchers explore this paradox.^[37]https://pubmed.ncbi.nlm.nih.gov/29061425/

2017 Research:

Valproic acid is often administered to patients undergoing radiation therapy for brain tumors to help manage seizures. Doctors note that delay or prevention of hair loss in this population seems to be a positive side effect.^[38]https://pubmed.ncbi.nlm.nih.gov/27889835/

1996 Literature Review:

A 1996 literature review finds that alopecia is a common side effect of treatment with antimanic agents, and is expected in up to 12% of patients undergoing treatment with valproate, and 10% of patients being treated with lithium.^[39]https://pubmed.ncbi.nlm.nih.gov/8899137/

1992 Case Report:

Two reports with seemingly conflicting results. In one, lithium-induced hair loss improved when lithium was replaced by valproate. In the other, hair loss improved only after stopping valproate.^[40]https://pubmed.ncbi.nlm.nih.gov/1486112/

Establishing Cause and Effect 

The above case studies offer evidence that the relationship between psychopharmaceuticals and hair loss may be more nuanced than expected.

Case reports are justifiably considered a weaker form of evidence. In other words, they rank low on the hierarchy of evidence. While case studies (i.e., n=1 published anecdotes) offer ‘signals’ for scientists to explore in future randomized controlled clinical trials, they also come with a high risk of bias. Case studies don’t establish prevalence rates, and it’s always possible that patients in these reports were using other medications and/or experienced additional life events that might also explain their hair loss. While they indeed contribute to future research, using case studies to interpret cause and effect is difficult.

The bottom line? It’s not always easy to say, ‘this drug causes hair loss.’

Hair loss can have many causes, making a causal relationship between a single drug and hair loss very hard to prove. In some of the above studies on SSRIs, researchers tried to hone in on this relationship by stopping treatment, seeing if the hair grew back, and then rechallenging the patient with the same medication to see if their hair loss then returned.

While this process occurred in a few of the case studies found, more research must still be done, as the sample size in the studies mentioned here consists of just a few people.

Another way to explore the existence of cause-and-effect is to dive more deeply into possible causes outside of the drug. Basically, one must rule out the following:

Are other medications present?

Patients receiving treatment for depression and anxiety may have other comorbidities or may be taking more than one medication.

Some of the case studies above report this, others make it clear the patient was an ‘exclusive user’ of the drug in question, while others make no such reference to either.

It’s possible that even in cases where one medication was discontinued and hair loss subsequently stopped, that it was the interaction between one or more drugs, and not a single drug, that triggered the onset of hair shedding.

Are other skin conditions present?   

Several of the studies on lithium, which is widely described as a drug which ‘causes’ hair loss, mentioned patients who had pre-existing skin conditions, particularly scalp psoriasis. While it may be true that they experienced alopecia only after beginning lithium treatment, the root cause of hair shedding could have been their psoriasis.

Several patients in the above case studies had also experienced alopecia in the past. Alopecia is an embarrassing condition which can lead to depression and anxiety. Also, those with depression and anxiety may be predisposed to alopecia. Researchers estimate that up to 30% of patients with skin conditions have psychiatric comorbidity.^[41]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7756276/

Is the patient trustworthy?

Of the case reports presented here, researchers often (but not always) confirmed the patient’s own reports of hair loss and hair regrowth. In just one instance was there mention of blood drawn to confirm the patient was indeed taking only the medication prescribed, as directed.

Particularly regarding the anti-anxiety medications, some patients presented with symptoms of schizophrenia. Hair pulling, or trichotillomania, must be ruled out in those cases and others.

Understanding the Mechanisms of Action

Understanding the mechanisms of action can also help establish cause and effect. While it’s still unknown exactly how these medications induce hair loss, the following are a sample of the most plausible theories. 

Melatonin and Hair Cycle Interruption

Psychotropic drugs typically cause diffuse, reversible alopecia by influencing hair’s telogen (shedding) phase.^[42]https://pubmed.ncbi.nlm.nih.gov/10798824/ The exact mechanism via which this works has yet to be revealed, although it may be connected to the relationship between serotonin and melatonin.

Serotonin is a precursor to melatonin, but the two also work in tandem to regulate a healthy circadian cycle. SSRIs in particular may decrease melatonin, which plays a role in hair cycle control.^[43]https://pubmed.ncbi.nlm.nih.gov/16217127/

Hypothyroidism

Lithium and other antimanic agents may exacerbate hypothyroidism. While lithium cannot seem to shake its reputation as a cause of hair loss, researchers do not necessarily believe that lithium is the direct cause. Rather, it seems that hypothyroidism (caused by lithium) is to blame. Insufficient thyroid hormone can trigger telogen effluvium.  

Dose Dependency

With lithium and some other psychopharmaceuticals, dosage plays a role in determining risk for hair loss. Some patients who experience hair loss may find that reducing their dosage allows their hair loss to abate. Lithium in particular, rarely has to be discontinued entirely.^[44]https://pubmed.ncbi.nlm.nih.gov/3157663/

Understanding more about the relationship between dose and hair loss may help researchers learn more about the mechanisms behind cause and effect.

Women vs Men

Hair loss related to psychopharmaceuticals is overwhelmingly experienced by women, not men. In one literature review, nearly 89% of the reports came from women.^[45]https://pubmed.ncbi.nlm.nih.gov/16783834/ Understanding why women seem to be more affected by this type of hair loss may offer clues into the mechanism of action. 

Multidirectional Relationships

Some drugs have a multi-directional relationship to hair loss, for reasons that aren’t yet entirely understood. Valproate and valproic acid, for example, can lead to hair loss when orally administered but may lead to hair growth when applied topically. In two of the case studies mentioned above, alopecia areata improved with paroxetine treatment, a drug that has induced hair loss in others.

These multidirectional relationships may shed light on cause and effect, but also, offer insight into how complicated it is to point to any one drug as a cause of hair shedding.

Hair loss, particularly telogen effluvium, may be related to trauma, stress, anxiety, or depression. Some people may find their hair loss improves as their anxiety and depression get better. On the other hand, researchers acknowledge it’s possible that cases of hair loss are underreported, either due to self-neglect or because the patient has experienced it in the past as a result of emotional stress and does not relate the occurrence to the drug.

What Can Be Done?

In general, the incidence rate for these reports of hair loss associated with antidepressants, anti-anxiety medications and mood stabilizers, appears to be quite low. It’s not a given that hair loss is an outcome with any of these drugs.

That said, hair loss can be devastating for the one person that experiences it. And in some cases, may lead to non-compliance with what otherwise are very effective and life-improving drugs. 

Before deciding to forego or discontinue treatment, it’s worth it to consider that in all the cases mentioned above, patients reported their hair shedding stopped after an adjustment to dosage, or once treatment ended. 

For those who have recently begun taking a new medication and have noticed hair thinning or hair shedding, it would be advisable to speak with a doctor about switching to another medication. Remember, there were several antidepressants and anti-anxiety medications that did not make the list because there was no evidence linking them to hair loss.

That said, if a medication on this list lands in the medicine cabinet, the risk of hair loss remains very low. 

Summary

It’s true there are case studies linking some psychopharmaceuticals to hair loss. But generally, the incidence rates are low, and hair loss tends to stop when dosages are lowered or the use of the drug is discontinued.

That said, for the individual experiencing hair loss, it’s of little comfort to know that risk is low. Maintaining healthy hair can be an important part of maintaining emotional and psychological health. If treating anxiety or depression is having a negative effect on hair, it may be time to talk to a doctor or dermatologist about an alternative treatment plan.

While happiness and health should always supersede hair growth, in this case, people shouldn’t have to sacrifice either.

Histamine and Hair Loss

Our hair follicles are part of a niche of cells intimately involved in proper immune function. For example, right next to the dermal papilla, the type of cell that grows our hairs, there are a number of immune cells including:

• Macrophage, which helps remodel our extracellular matrix and clean up waste.
• Basophils, which help neutralize foreign particles.
• Neutrophils, which keep pesky microorganisms present on our scalps, in check.
• And in reference to today’s topic, Mast cells which secrete histamine to neutralize foreign invaders. 

Mast cells can become counterproductive though when too much histamine is secreted. They induce immunoglobulin secretion by our B-cells (those same cells that act as antibodies to viruses), such as the release of IgE – the same immunoglobulin that can create anaphylactic shock. 

Histamine is also a pro-inflammatory cytokine (a signaling molecule), that can generate a number of unwanted cell responses that tend to progress hair loss. 

In this article, we take a look to see just how much are mast cells and histamine to blame for hair loss, and what can be done about this. We also take a look at the evidence for the use of antihistamines as a hair loss reversal tool.

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What Is The Role Of Histamine In Hair Loss?

How Histamine Works

Histamine is counterintuitively not a hormone, instead, it’s actually a simple amino acid. We get histamine thanks to consuming its precursor amino acid histidine. And it is vitally important for maintaining normal physiology.

Histamine also binds to four receptors. Some of which are located on our skin, some in our gastrointestinal system, and some in our brain. Histamine in the brain is also important for acting as a neurotransmitter.

It’s the excess of histamine signaling that becomes problematic.

A perfect example of excessive histamine signaling being bad is in the case of seasonal allergies, or food allergies. Anyone who has had experience will know how quickly and fiery the body responds to these allergens. This is all due to the release of histamine and how it interacts with those receptors.

With excess histamine signaling, people become easily irritated and prone to inflammation. Body temperature also increases and the vascular system becomes more permeable, causing immune cells to leak into unwanted places.

This opening of our vascular system and leaking of immune cells in unwanted places is actually one way histamine connects to hair loss.

The Histamine-Hair Loss Connection

Because hair follicles and scalp act as a breeding ground for a variety of microorganisms, it is also very prone to exacerbated histamine signaling if the scalp biome balance is thrown off. Further, because histamine responds to changes in hormone levels, it’s very possible that the shift experienced with androgenic alopecia also increases histamine production.

Both androgenic alopecia and alopecia areata also show signs of dysregulated histamine signaling. Histamine in excess can induce pro-inflammatory cascades that cause premature apoptosis of cells, especially as it relates to the dermal papilla.

This rapid apoptosis can extend to cells (such as stem cells) sitting on our epidermis. Stem cells in the subcutaneous tissue and on the hair follicle’s outer root can bulge. Premature apoptosis of these cells makes it increasingly difficult to regrow hair since the stem cells which contribute to hair renewal are no longer present.

The Evidence For Histamine Contributing To Hair Loss

While the discussion on histamine specifically is rather sparse in relation to hair loss, there have been some advances in the past years on the role of histamine overall. For example …

• When humans experience stress, the body tends to release histamine in much larger amounts. This excess of histamine is believed to affect our hair follicles and act as part of the pathophysiology of stress-induced telogen effluvium. In the following study, patients with telogen effluvium had significantly higher numbers of mast cells and the enzyme tryptase.^[1]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5514792/.

Tryptase is an enzyme involved in the degradation of proteins, specifically by removing lysine, histidine, and arginine. Higher tryptase is also a hallmark of mast cell activation.

•  Alopecia areata is one of the more commonly accepted forms of hair loss due to the immune system going awry. In alopecia areata, there is a large change in immune function due to the loss of immune privilege. Immune privilege is a mechanism the body uses to keep immune cells out of certain sensitive tissues.

When the hair follicles experience a collapse of immune privilege, they also experience a dramatic increase in a variety of immunological factors. Specifically, a rise in lymphocytes like CD8+ T-cells, and IgE. Both of which are either triggers/ secrete (T-cells) histamine or can be triggered by histamine release from mast cells.

Specifically, the deep perivascular and perifollicular regions of those with alopecia areata, when compared to controls, had higher CD4+ T cell count, and CD8+ T cell count. They also had more mast cells.

These findings reached multiple orders of magnitude in terms of significance. Interestingly, this was not really something of concern when it came to the upper dermal region. Indicating that unless we look further down the dermis, we are unlikely to see any noticeable changes in immune profiles. 

• Androgenic alopecia is often discussed as only ever being due to the increase in androgen signaling. Specifically, the production of DHT from testosterone via the 5AR enzyme and its binding to the androgen receptor. However, what isn’t often discussed is what happens afterward? 

It’s not as if the androgen and the androgen receptor are initiating hair loss. Instead, the androgen receptor with DHT translocates into our cell’s nucleus and then tells the cell to change genetic expression. Some of those genes (but not all), happen to be genes for the production of extracellular matrix. 

This can lead to the overproduction of elastin, leading to a feeling of hard tissue often referred to as fibrosis of the scalp. In another case-control study, the increase in collagen fibers, elastin, and the lower diameter of hair follicles, was apparently clear in those with androgenic alopecia.^[2]https://pubmed.ncbi.nlm.nih.gov/18286292/

Figure (a) and the graph to the right of it are indicating the increase of collagen bundles in the occiput and vertex of either controls or those with AGA. While the occiput didn’t differ much, the vertex was clearly different.

Figure (b) is indicating the increase in elastin seen in those with androgenic alopecia as compared to control.

And when it came to mast cells, those with androgenic alopecia also had a higher level of the enzyme tryptase (again indicative of mast cell activation). Interestingly, tryptase is also a well known factor involved in the activation of TGF-ß and collagen remodeling, potentially pointing to a role of mast cells in the fibrosis of those with AGA. 

It’s important to keep in mind that these findings were for a total of 10 patients and 5 controls. A greater sample size range is required to definitively tell if this is either a correlation or a fluke. 

Interestingly, the increase in TGF-ß signaling appears to be contradictory when it comes to alopecia areata. In androgenic alopecia it’s implicated as a fibrosis-inducing agent, while in alopecia areata, the loss of TGF-ß is a precursor step to loss of immune privilege. 

This change in activity of TGF-ß is known to be induced by a shift in mast cells from an immune-inhibitory role to a pro-inflammatory role.^[3]https://pubmed.ncbi.nlm.nih.gov/24832234/

One research group had actually investigated this separately with a mice model and determined with incredible accuracy that one of the reasons for the differential response of mast cells as either good or bad, is partly due to the scalp microbiome and dermal fibroblasts.^[4]https://pubmed.ncbi.nlm.nih.gov/30928651/

The mice study showed that the scalp microbiome activates toll-like receptors (a type of immune recognition receptor) and amplifies progenitor cells from the keratinocyte to become mast cells. Further, a change in how the mast cells behaved was seen. One of immune inhibition into one of pro-inflammation and immune cell recruitment. 

It’s possible that for alopecia areata, a change in how the scalp microbiome interacts with immune cells is the prelude to the disease. While with androgenic alopecia, a change in how mast cells behave is a prelude to premature apoptosis of the dermal papilla cells. 

Do Antihistamines Work Against Hair Loss?

The next step in assessing the role of mast cells in hair loss is to consider if anyone has looked at the use of antihistamines for hair loss. After all, while mechanistic and observational data connecting histamines to hair loss are important, interventional studies are really the only way to ascertain cause and effect.

Luckily, there are some research papers that addressed this question.

The first study investigated the antihistamine drug cetirizine (if you’ve ever tried claritin or zyrtec, this is the same active ingredient), because of its known inhibitory actions on histamine-1 receptors and PGD2 (a proinflammatory prostaglandin shown to worsen androgenic alopecia).^[5]https://onlinelibrary.wiley.com/doi/abs/10.1111/jocd.13940    

What the authors did was give 30 participants a 1% solution of topical cetirizine at 1mL doses. The second group which served as a control group was given a placebo solution. After six months these were the results:

Essentially, the control group showed no improvement with 4/30 of them seeing worsening responses. While the treatment group saw sparse improvements in photographic assessments and self assessments. Nothing too crazy, but still better than the control group.

In a second study, researchers compared 1% cetirizine vs. 5% minoxidil. In this randomized controlled trial, both groups saw great results in terms of hair density, hair diameter and other hair loss parameters. Minoxidil however, outperformed topical cetirizine.^[6]https://journals.library.ualberta.ca/jpps/index.php/JPPS/article/view/31456/21623

This is expected since minoxidil works by promoting the anagen phase of hair follicles. Cetirizine simply works by blocking the uptake of histamine in the histamine-1 receptor. This is fascinating to note though as by simply blocking the cellular actions of histamine, cetirizine has comparability to minoxidil. 

Their outcomes showed some of the following features:

1. Although baseline levels of hair density were higher in the minoxidil group, the cetirizine group had close efficacy. Keeping up with the results of the minoxidil group.
2. Minoxidil had better results in terms of vellus hair density, despite starting with a higher baseline. And minoxidil had equal efficacy as cetirizine did in regards to terminal hair density. 
3. Cetirizine group had a greater reduction in telogen hair follicles 16-weeks in compared to minoxidil. But this effect rebounded slightly during the 24-week mark. Why this is the case is hard to determine. 

Nonetheless, a combined therapy may be even more potent at addressing hair loss… 

In the final study on cetirizine, patients were once again administering 1mL of a 1% solution of cetirizine topically. After six months, a dramatic improvement in hair regrowth was seen for the participants when compared to the control group.^[7]https://pubmed.ncbi.nlm.nih.gov/28604133/

The top row indicates the beginning of the study for the participants. While the bottom row indicates the end of the study. A clinical difference can be seen in all of the patients’ hairlines. In all cases, there were no known side effects too.

What’s Our Take On The Data?

There is a clear rationale for the induction of mast cells in the pathology of possibly all forms of hair loss, including a connection to immune defects like telogen effluvium. Mast cells play a critical role in feedback from the scalp microbiome to our scalp cell niche. 

When mast cells go awry, they release histamine, tryptase, and a number of other factors that cause extracellular matrix remodeling, recruitment of immune cells, and a vicious cycle progressively worsening with time. 

Addressing the excess histamine production by interfering with the histamine-1 receptor with cetirizine, abrogates most of the negatively associated responses and actually does seem to allow regeneration of hair follicles. 

Based On The Evidence

The use of topical cetirizine can be a very appropriate tool to implement with androgenic alopecia and alopecia areata. The rise of mast cells and the enzyme tryptase in patients with telogen effluvium as compared to controls also provides a very compelling argument as to how stress correlates with hair shedding disorders.

It is with the totality of the current evidence, prior knowledge on the mechanisms of mast cells and their roles in our bodies, as well as the efficacy of antihistamines in improving hair loss, that we believe the weight of the evidence largely supports a causal role of mast cells in the development of various forms of hair loss. 

What Then Should Be Done?

Since topical cetirizine consistently shows a net benefit in all the current clinical trials, the most logical addition should be topical cetirizine for any hair loss disorder. It may be that in conjunction with minoxidil, large improvements can be acquired. 

Further, with topical anti-inflammatories, cetirizine can dramatically reduce the apoptosis rate of precious stem cells surrounding our hair follicles. There are alternatives to cetirizine that operate in similar mechanisms, reducing histamine release and subsequent binding to histamine-1 receptors.

Some of the useful ingredients that can reduce histamine production and the effects of histamine include: 

• Vitamin B6.
• Copper.
• Vitamin C.
• Iron. 
• Vitamin D.
• Ginger.
• Garlic.
• MSM.

And many more. A majority of the micronutrients and vitamins are also key cofactors for proper function of the enzymes involved in histamine degradation – such as Diamine oxidase and Histamine-N-Methyl Transferase enzymes. 

Product Recommendations

Although we can’t generally acquire topical cetirizine, one can be made by dissolving 1 g in 100mL of water. Forming 1% w/v cetirizine, just as outlined in the studies. The only difference would be that the study used a form of alcohol instead of water. 

A simple formulation you can make at home includes: 

• Take 1 g of Cetirizine, crush it in a mortar, and pestle very finely. 
• Dissolve it in 100mL of water.
• Add 1-5mL of ethyl alcohol (70-90%). 
• Add 1-5mL of Coco glucoside to help with absorption, or more depending on the consistency you would like.
• Thoroughly mix the ingredients and store it in a dark brown bottle with a 1mL serving pump.

*Note: If you plan on using oral antihistamines, remember that they distribute widely throughout the body, not just the skin. The compounds prevent histamine from binding to the brain which is one of the reasons for the drowsy feeling many experience with Zyrtec or Claritin.

To some extent, every hairline is unique. But there are identifiable hairline patterns, primarily based on age, gender and genetics. As men age, their hairline will typically recede a bit, known as ‘maturing.’ While this can understandably make men nervous, it’s not always a sign of male pattern balding. In this post, we’ll review the following:

• What defines a mature hairline
• What defines a receding hairline
• The difference between a mature and receding hairline
• How to treat a receding hairline

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What is a Mature Hairline?

The hairline is the boundary between hair follicles and the forehead. Everyone’s hairline is unique, although there are some patterns that occur throughout our lives. 

According to observational studies, prepubescent men and women both experience concave shaped hairlines. This generally concave hairline is similar across all races and ethnicities. Around the age of 10, a small percentage of children develop a widow’s peak, but this is not an effect of recession at the temples.^[1]https://www.researchgate.net/publication/256479799_Phenotype_of_Normal_Hairline_Maturation

Full citation: Rassman, William & Pak, Jae & Kim, Jino. (2013). Phenotype of Normal Hairline Maturation. Facial plastic surgery clinics of North America. 21. 317-24. 10.1016/j.fsc.2013.04.001.

As young teens, when hair is fullest, there’s typically a stark boundary between the hair on the head and the forehead. In men especially, this changes with age. It’s believed that hormonal changes trigger the expression of certain genes, causing men’s hairlines to mature between mid-adolescence and middle-age. This maturation means the hairline shifts a few centimeters further back on the forehead.

This shift may take place uniformly, following the rounded shape of the juvenile hairline, or may be more noticeable at the temples, resulting in a hairline that looks more like a letter M. There appears to be a relationship between the muscles of the forehead, the frontalis muscle, and the height of the hairline. Most adults with high mature hairlines have presented with high foreheads their entire lives. The varying degrees of normal hairline maturation can be seen in the image below. 

As hairlines mature with age, some men hardly notice this change, as it occurs slowly over a period of 10 years or more. In others, this change happens more rapidly, causing concern.

Regardless of when or how quickly it happens, what characterizes a mature hairline is that the recession is limited to just a few centimeters, and then it stops. The hairline does not continue to recede, and remains well-defined, with little to no hair thinning.

A maturing hairline is a natural part of aging, and not indicative of androgenic alopecia (AGA), otherwise known as male pattern baldness. 

At What Age Does Mature Hairline Stop?

If and when a juvenile hairline begins to recede, the most commonly asked question is – when does it typically stop? 

Just as there’s no telling if and when the hairline will mature, there’s no predicting when a mature hairline will stop. A slightly different, but better question is – how do you differentiate between a maturing hairline, which will eventually stop receding, and receding hairline, which is a sign of male pattern baldness? 

To answer this, we begin with an understanding of receding hairlines.

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What is a Receding Hairline?

A receding hairline is among the earliest signs of androgenic alopecia. AGA often follows a predictable pattern. This pattern begins with a receding hairline, which is especially noticeable at the temples. Simultaneously or sequentially, hair then disappears from the crown of the head. Eventually, complete baldness occurs as the hairline recedes far enough back, and/or baldness from the crown of the head meets the hairline.

The Norwood-Hamilton scale is used by dermatologists to assess progression of AGA. By stage 2, minor recession of the hairline exists, although it’s barely differentiated from a maturing hairline.  By stage 3, the hairline has receded much further at the temples, characteristic of androgenic alopecia.

What Causes a Receding Hairline?

Hair shedding is a common part of the normal hair growth cycle. Most people lose somewhere between 50-100 hairs each day, which typically goes unnoticed. When hair loss is localized to the front of the scalp and regrowth does not occur, the hairline recedes.

Age, genetics, gender, hormones, or how you care for and style your hair can all contribute to a receding hairline. 

Age: While AGA can occur in children, it’s very rare. Most of the hairline changes that occur with age are not reflective of AGA, until after the age of 17. As we age, the chances of developing a receding hairline increase. Androgenic alopecia is more common in those who are middle-aged or older.

Genetics: Research suggests that there is no single gene involved in AGA. Rather, pattern hair loss is likely a polygenic disorder, meaning there are many gene variances that are involved in the predisposition of its development. Exactly which genes are responsible is still unknown, although a family history of androgenic alopecia is still its single greatest predictor. 

Gender: Men are more likely than women to have a receding hairline. Although women do experience AGA, it more often presents as overall hair thinning and baldness that begins at the top of the scalp, and not a receding hairline.

Hormones: While the hormone dihydrotestosterone (DHT), is responsible for growth of hair on the body, this testosterone derivative also contributes to hair follicle miniaturization, and ultimately, hair loss. Although it’s unknown why AGA forms the pattern it does, the answer might have to do with androgen receptor density and 5α-reductase activity at the hairline. 

Lifestyle: The onset of a receding hairline may be accelerated from certain forms of stress, medications, scalp environment, and/or hair styling — such as pulling hair too tight. Hair loss may arise from hormonal conditions unrelated to DHT, such as hypothyroidism or hyperthyroidism. Gut dysbiosis, heavy metal toxicity, and vitamin deficiency can all contribute to hair loss.  

Unlike maturing hairlines, receding hairlines are not part of the normal aging process, but a sign of androgenic alopecia, another form of hair loss, or both.

Mature vs Receding Hairlines

A mature hairline doesn’t always become a receding hairline. So what indicates the difference between the two, and how can we tell the difference between early AGA and a simple shift in the hairline? 

Timing of Hair Loss: Hairlines tend to mature in late adolescence or early adulthood. Generally, receding hairlines start later in life.

Pace of Hair Loss: A receding hairline tends to progress at a faster pace. While a maturing hairline may go unnoticed – a receding hairline is more likely to attract attention.

Shape of Hair Loss: A receding hairline tends to move more towards an M-shape, with hair loss at the temples far more pronounced. A mature hairline, on the other hand, will move back more evenly.

Extent of Hair Loss: As the hairline matures, it may move back 1-2 centimeters. With a receding hairline, this shift can be 1 inch or more. 

Thinning of Hair: As a hairline matures, hair maintains its original thickness. Receding hairlines, on the other hand, are accompanied by hair thinning.

Diagnosing a Receding Hairline

A receding hairline is characteristic of androgenic alopecia, but it’s possible to have more than one type of hair loss, especially if the hairline is receding and hair is thinning or balding in other areas.

In the shower, when washing your hair, take all the hairs you shed onto your hands and stick them to the wall using the steam from the shower. 

• Are the hairs of varying diameters? This is indicative of hair follicle miniaturization, a defining characteristic of AGA.
• Are the hairs all equal in thickness? This suggests no hair follicle miniaturization, and an AGA diagnosis is less likely. You could have a hair shedding disorder.

A doctor or dermatologist can help identify exactly which type of hair loss is present. This is important, for treatment protocols will vary depending on the cause of hair loss. 

How to Prevent Further Receding

There isn’t one single solution for hair loss, which makes diagnosing the cause and type of hair loss important. But in general, a comprehensive solution will address the following:

1. Regrowth Regimens: Depending on personal preferences, this could include medications or other science-based hair regrowth regimens.
2. General Health: This includes specific dietary and lifestyle interventions based on age, gender, and type of hair thinning to address any conditions linked to the hair loss. While poor general health may accelerate hair loss, for most people, it’s very much a secondary factor in terms of influence over a receding hairline.

Of course, no treatment is always an option. Many choose to change hair styles in an effort to hide a receding hairline, or are comfortable living with it as is. If choosing treatment, factors to consider include how much time and money to invest on hair regrowth, tolerance for side-effects, and personal preference. 

A few possible interventions are listed below (and not in order of importance or clinical efficacy).

Massaging: Massaging the scalp for 15 minutes, twice daily has the ability to activate the body’s innate healing responses, and reduce scalp tension. Our own study showed that 75% of people who massaged consistently for 8 months reported a stop or partial reversal in their hair thinning.^[2]https://link.springer.com/article/10.1007/s13555-019-0281-6

Shampoos: Ketoconazole shampoo is not actually FDA-approved for pattern hair loss, but is a popular treatment for the condition nonetheless. It’s not yet very well studied, but may work well in combination with other therapies.

Natural Topicals: Jojoba, castor, rosemary, peppermint, and saw palmetto extract are just a few of the natural essential oils that have been marketed for hair regrowth. There are a few small studies showing that natural topicals may improve certain hair loss disorders.

Microneedling: Microneedling the scalp to treat hair loss is typically done biweekly. Microneedling evokes very low levels of inflammation which evoke a healing response from the body. Studies show microneedling can be successful when done alone, or when performed alongside other therapies. ^[3]https://www.tandfonline.com/doi/abs/10.1080/14764172.2017.1376094?journalCode=ijcl20

Low-Level Laser Therapy: Low-level laser therapy (LLLT) is perhaps the most popular non-drug hair loss treatment and has FDA-clearance as a hair loss treatment for both men and women. The expensive and time consuming treatment does improve hair count for those with AGA.

Medications: Minoxidil and Finasteride are the only 2 FDA-approved medications for hair loss. Each treats AGA either orally or topically. While these medications have been proven effective to treat hair loss, they’re not for everyone. Both lead to side effects in some people, and generally require life-long use.

Botox: Botox is a neuromodulator which relaxes muscles and may also reduce certain inflammatory signaling proteins. Over the last decade, a few studies have been published measuring the hair-promoting effects of Botox on men with AGA.

Platelet-Rich-Plasma Therapy: Platelet-rich plasma therapy (PRP) is offered by thousands of dermatologists as a natural intervention for all types of hair loss. It is effective for androgenic alopecia and alopecia areata, but also expensive and ongoing  injections are required to maintain results.

Stem Cell Therapy: Stem cell therapy is an expensive; relatively new therapy that is still under investigation. It’s also not a one-and-done treatment and requires multiple appointments. Early findings seem to suggest that 90% of subjects respond to stem cell therapy. And for AGA subjects, increases in hair count seem to hover around 20-30%.^[4]https://pubmed.ncbi.nlm.nih.gov/31111157/

Effective treatment protocols often include some combination of the above. For example, studies suggest microneedling + minoxidil + finasteride, offers a response rate of 80-90% – with hair count increases ranging from 25-40% within 6-24 months. 

Summary

As a man’s hairline matures, it will recede slightly from its juvenile position. This can be alarming, but it’s not always an early sign of male pattern baldness.

A receding hairline differs from a maturing hairline in that it may recede at a much faster pace, recede further back, and will recede more at the temples than in the center, resulting in an M-shaped hairline.

A receding hairline is characteristic of androgenic alopecia, but could be related to other types of hair loss too, especially if hair is thinning or balding in other areas.

Diagnosing a receding (vs maturing) hairline allows treatment to begin before baldness further progresses. Treatment options which have been proven effective include massaging, microneedling and medications. Efficacy improves when these methods are combined.