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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.

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.

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%.

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.

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.

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)

Not a member? Sign up today to become part of the Perfect Hair Membership Community. You’ll gain instant access to a customized hair regrowth plan, 50+ guides, 30+ product reviews, 60+ case studies, community support forums, expert interviews, and more.

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.

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.

Introduction

Finasteride is one of the most commonly-prescribed medications for treatment of male pattern hair loss—also known as androgenic alopecia (AGA). But it’s also used as an off-label treatment for female pattern hair loss. Evidence suggests this medication can help regrow hair in both sexes.

But what’s the best dose of finasteride for women with AGA? Unfortunately, it’s complicated. This article sets out to evaluate the data, uncover the answers, and provide recommendations based on the current landscape of clinical research.

What Is Finasteride?

Finasteride is a drug developed to inhibit type II 5-alpha reductase. This is an enzyme in the body that converts free testosterone in dihydrotesterone (DHT).

Essentially, finasteride lowers DHT levels by reducing the amount of type II 5-alpha reductase circulating throughout our bodies. And by taking finasteride at 0.2 to 5.0 mg daily dosages, we can often reduce total DHT levels by 70%. ^[1]https://www.ncbi.nlm.nih.gov/books/NBK513329/

Why Use a Drug To Reduce DHT?

DHT is not just a metabolite of testosterone; it’s also the primary male hormone causally associated with androgenic alopecia.

We know this because studies have shown that men who cannot produce DHT are nearly fully-protected from going bald throughout a lifetime. Furthermore, clinical studies on DHT-lowering drugs – such as finasteride – show that if DHT levels are suppressed enough, 80-90% of men can arrest the progression of their pattern hair loss and even regrow 10-20% of their lost hair. ^[2]https://pubmed.ncbi.nlm.nih.gov/29407002/ ^[3]https://www.ncbi.nlm.nih.gov/books/NBK430924/

Similarly, studies on females with androgenic alopecia have shown that finasteride can also improve their hair loss outcomes. The evidence is less robust than for men, but finasteride is something many women should consider trying in order to improve their pattern hair loss.

Finasteride for Women: What’s the Perfect Dose?

In men, the FDA has approved the use of 1mg of finasteride for pattern hair loss. However, male and female hair loss cases are not always the same. Reducing DHT levels is often of therapeutic interest to fighting AGA – and for both sexes – but some clinical evidence suggests that females might need a different dose of finasteride versus males.

How Much DHT Does Finasteride Reduce?

Finasteride has what is known as a dose-dependent, logarithmic response curve for DHT reduction. In other words: a little bit of finasteride reduces nearly as much DHT as a lot of finasteride. For an example, see this chart:

Clinical studies have demonstrated that 0.2 mg and 5.0 mg reduce nearly the same amount of finasteride: 69% versus 72%, respectively.

Because of this, a lot of people actually prefer to use lower dosages of finasteride than what is generally prescribed. This practice is also supported by clinical data. For instance, in men, 0.2mg of finasteride AGA at a statistically similar level as 1.0 mg of finasteride over the course of a year. ^[4]https://europepmc.org/article/med/15319158

But is the same true with females? Unfortunately, the data is less clear.

Finasteride for Female Pattern Hair Loss: the Clinical Evidence

The FDA approves the use of 1 mg of finasteride for male pattern hair loss.^[5]https://www.fda.gov/drugs/information-drug-class/5-alpha-reductase-inhibitor-information But the underlying causes of male and female pattern hair loss cases (androgens such as DHT) are not always the same. Furthermore, while reducing DHT levels is of therapeutic relevance in treating AGA in men and women, some clinical evidence suggests that females might need a different dose of finasteride versus males. 

What does the available research tell us? Here are a few of the key studies on finasteride for women, and their main findings (summarized in the table below).

Finasteride for Women: Key Studies

Finasteride for Women: Key Studies Takeaway

There is conflicting data regarding the efficacy of finasteride for female pattern hair loss. Some studies report improvements while others do not.

There are some key variables to consider when weighing the available evidence:

• The dose of finasteride used
• The length and frequency of treatment
• Oral administration versus a topical treatment
• Whether finasteride was used in conjunction with other drugs or therapies
• The type of hair loss in the patient groups (e.g., female pattern hair loss versus age-related thinning – and was this accurately determined?)
• Patient age, history, and status (e.g., pre-, or post-menopausal, or abnormal androgen levels)
• How the treatment was assessed (e.g., quantitative hair counting versus patient self-assessment)
• Whether the study contained appropriate controls (i.e., placebo-receiving patients, ideally matched for age, weight and medical history)
• The number of patients in the study (which affects the statistical power; was the study a case report of one patient, or a larger study with a control group?).

Interpreting research data can be difficult and confusing. such as different studies using different dosages of finasteride and for varying lengths of time, measuring different hair loss outcomes, and using different numbers and ages of patients.

The specific type of hair loss is also a crucial variable.^[19]https://pubmed.ncbi.nlm.nih.gov/30604525/  Often, studies reporting positive outcomes are based on patient self-reporting, which can be suspect and not meaningfully objective or quantitative in measuring true prevention or reversal of hair loss.

What is the best dose? Explaining the conflicting results.

Given the dose-response relationship between finasteride and DHT levels, shouldn’t 1 mg be as effective as 5 mg? Why aren’t women getting consistent regrowth across doses within these ranges?

Other discrepancies are the time for which finasteride was given. In men, 1 mg of finasteride can be effective in 6-12 months, but it is possible that women require more long-term treatment regimens.^[20]https://pubmed.ncbi.nlm.nih.gov/30604525/ Generally, success with finasteride in women has been reported in both the short- and long-term.^[21]https://pubmed.ncbi.nlm.nih.gov/12399766/

Alternatively, the difference in observed efficacies between studies may be due to patient background and the type of hair loss. Hair loss in patients suffering from PCOS or adrenarche (i.e., high levels of adrenal gland activity) likely has a clear causal link to abnormal androgen signaling (and therefore suitable for finasteride), where hair loss in post-menopausal women may be more akin to age-related hair ‘thinning’, and not linked to testosterone or DHT, which may explain why some studies find no effect with finasteride.^[22]https://pubmed.ncbi.nlm.nih.gov/10674382/^[23]https://pubmed.ncbi.nlm.nih.gov/11050579/^[24]https://pubmed.ncbi.nlm.nih.gov/12399766/

That said, finasteride is also reportedly effective in patients that are androgen-normal.20 Therefore, there needs to be more careful classification of the type of hair loss and the likely underlying mechanisms, as well as clear standardization of treatment outcome measurements. 

Conclusions

Does finasteride work for women suffering from hair loss? If so, what is the ideal dosage? 

Finasteride is most beneficial for women when their hair loss occurs alongside elevated androgen levels—much like hair loss in men.

It is likely that DHT is a major factor in a proportion of female hair loss cases. Finasteride is likely to be a beneficial part of a successful hair loss regimen in these cases. However, it is not clear that male and female pattern hair loss universally share the same underlying cause.

Finasteride may be less suitable in contexts of age-related hair thinning. Hair follicles are sensitive to all manner of different hormones and chemical signals, not just androgens such as testosterone and DHT.^[25]https://pubmed.ncbi.nlm.nih.gov/32731328/

The best dose is one that maximizes the desired benefits (prevention and reversion of hair loss) while minimizing any undesirable side effects.

Finasteride can be effective at reducing DHT even in small doses. Because of this, experimentation with low levels of finasteride may lead to results with far less exposure to chemicals. Topical treatments may also be considered to further reduce systemic side effects.

Therefore, the best dose will be patient-subjective. Prior consideration of your history, goals regarding hair loss, and experimentation with dosages is needed before you will find the ideal routine for your hair health.

Latanoprost is a medication that was originally developed to treat glaucoma. Over the last two decades, research groups have also started testing it as a treatment for hair loss – including alopecia areata, androgenic alopecia, and telogen effluvium.

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.

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?

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.

If you’re experiencing hair loss, and you’re searching for a solution to help regrow hair, you’ve likely read several articles that reference different parts of the scalp. But what would you say if you were asked where on your scalp you’re losing hair? And how well do you understand the various parts of the scalp that lay beneath the skin, as well as their roles in hair loss?

In this article, we’ll give a quick introduction to the scalp. After that, we’ll take a tour of the scalp, starting with the different regions on the surface; then moving beneath the skin through the various layers of scalp tissue; then exploring the bones that lay beneath the tissue; then discussing the arteries, veins, nerves, and lymph vessels than run through those layers of tissue; and then examining the muscles that pull on the scalp. After touring the different areas of the scalp, we’ll discuss some ways that scalp mechanics may impact hair growth. Finally, we’ll look at some clinical evidence that has opened up the possibility of new treatments for androgenic alopecia. 

Introduction to the Scalp

The scalp consists of layers of skin and subcutaneous tissue that cover the human cranium. It extends from the supraorbital foramina (i.e. two openings in the bone just above the eye sockets and just beneath the eyebrows) to the superior nuchal line (i.e. one of four curved ridges on the exterior surface of the occipital bone, which lies at the back of the head). It is bordered on the front by the face and on the sides and back by the neck. 

The scalp acts as a physical barrier to protect the cranium against physical trauma and potential pathogens. It is also the area where human hair typically grows in order to 1) aid in heat conservation, and 2) play a role in aesthetic appearance and sexual signaling.   

A Tour of Your Head: Regions of the Scalp

If someone were to ask you where on your scalp you’re losing hair, would you know how to answer them? If you’re unsure how to answer that question, check out the descriptions below.

The surface of your head has seven main areas, or regions, which are described below:

• Temples: The temples are located on either side of the head, behind the eye and between the forehead and ear. Each of the two temples is a latch where four skull bones – the frontal, parietal, temporal, and sphenoid bones – fuse together. Male pattern baldness typically starts at the temples, then continues to recede into the scalp, resulting in an M-shaped hairline. 
• Frontal Region: If you were to draw an imaginary vertical line through your head, with the line positioned just in front of your ears, that line would demarcate the border between the frontal and mid-scalp regions. The part of the scalp that lies in front of that line is the frontal region. Also called the forelock, this region includes the hairline and the hair above the temples. If you’re losing hair due to male pattern baldness, this is often one of the first places you can expect to see hair loss. 
• Mid-Scalp Region: If you were to draw two imaginary vertical lines through your head, with the first line positioned just in front of your ears and the second line positioned just behind them, the relatively flat area between those two lines would be the mid-scalp region. Unless you’re at an advanced stage of male pattern baldness, you probably won’t experience much hair loss in the mid-scalp region.  
• Vertex Transition Zone: Also called the vertex transition point, this area is located between the mid-scalp region and the vertex. The vertex transition zone is the area where the scalp goes from a horizontal to a vertical plane posteriorly. For this reason, it is often referred to as the posterior hairline. Although this area is technically part of the vertex (see next bullet), it is often listed as a separate region. 
• Vertex (Crown): Also called the crown, the vertex is the highest point on your scalp (the word “vertex” literally means “highest point”), which is located towards the back of your head. On non-balding heads, the vertex is typically identified by a swirl pattern of hair. In addition to losing hair around the temples and in the frontal region, many folks see noticeable hair loss on the crowns of their heads. 
• Sides (Temporal Regions): Also known as the temporal regions (because they sit over the temporal bones and muscles), these are the areas on either side of the head that are positioned just above and behind the ears. Because the sides of the head have a different subcutaneous anatomy than the rest of the scalp, they are sometimes treated as separate from the scalp. However, the temporal regions generally grow hair, so we’ve chosen to include them in this tour of the scalp. Hair loss is much less common in this region. 
• Back (Occipital Region): Also known as the occipital region (because it sits over the occipital bone and muscle), this area covers the back of the head, underneath the crown. As with the sides of the head, hair loss is much less common in this region. 

Digging into the Anatomy: Layers of the Scalp

While the previous section provides a good overview of the various areas on the surface of the scalp, there is a lot more going on beneath the surface.

The scalp consists of the following five layers:

1. Skin: The first layer of the scalp is the skin, which acts as a protective barrier to the rest of the scalp, helps prevent the loss of moisture, and helps regulate body temperature, among other things. This layer is thick and contains numerous hair follicles and sebaceous glands (i.e. small, oil-producing glands).
2. Dense Connective Tissue: The second layer is the dense connective tissue layer, which connects the skin to the galea aponeurotica (described below). In addition to connective tissue, this layer contains arteries, veins, nerves, and lymphatic vessels. Hair follicles can also extend from the skin down into this layer. 
3. Galea Aponeurotica: Also known as the epicranial aponeurosis, the galea aponeurotica is a layer of dense, fibrous connective tissue that runs along the top of the cranium, connecting to the frontalis muscle at the front of the head and the occipitalis muscle at the back of the head.

The first three layers of the scalp are firmly attached to each other and move as a unified structure. 

1. Loose Areolar Connective Tissue: This layer forms a flexible connection to both the galea aponeurotica and the pericranium (described below), allowing the top three layers of the scalp to slide over the lower pericranium. The loose areolar connective tissue also contains numerous blood vessels. 
2. Pericranium: Composed of dense connective tissue, the pericranium is the deepest layer of the scalp, which tightly adheres to the calvaria (i.e. the bones that form the top of the skull). It also contains the vascular supply that’s essential to supporting the calvaria. 

The Scalp’s Foundation: The Calvaria and Other Cranial Bones

As noted above, the pericranium is firmly attached to the calvaria bones, which form the top of the human skull. In addition to the calvaria, there are some other cranial bones that play a role in scalp function. We discuss these bones below.

The neurocranium, which is pictured in the image above, consists of the upper part of the skull that surrounds the cranial cavity and contains the brain. There are eight bones that make up the neurocranium:

• The frontal bone forms a skeletal roof above the eye sockets and nasal cavity, and forms the main part of the forehead. 
• The left and right parietal bones sit behind the frontal bone. These bones form the top and sides of the cranium.
• The occipital bone forms the back and base of the skull. It has a large opening, called the foramen magnum, where the spinal cord passes into the skull.  
• The left and right temporal bones help form the sides and base of the skull, where they protect the temporal lobe of the brain and surround the ear canal. 
• The sphenoid bone is situated in the middle of the skull towards the front. It helps form the base and sides of the skull, and has a shape that resembles a butterfly. 
• The ethmoid bone is a cube-shaped bone located in the center of the skull between the eyes. It helps form the walls of the eye sockets, as well as the roof, sides, and interior of the nasal cavity.

Although these are eight individual bones, they are joined together by various fibrous sutures.  

The neurocranium can be further divided into an upper and lower part:

• The upper part, known as the calvaria, consists of the flat bones of the skull that form a dome-like roof. This includes the frontal bone, parietal bones, and occipital bone.
• The lower part, known as the cranial base, includes the lower parts of the frontal bone, the sphenoid bone, ethmoid bone, temporal bones, and the lower parts of the occipital bone. 

Because the calvaria makes up the top part of the skull, these bones are more significant when discussing hair growth/loss. However, the muscles that attach to the temporal and sphenoid bones may also play a role in hair loss (more on that in a bit).

The Vertical Layer: Arteries, Veins, Nerves, and Lymphatic Vessels

We previously discussed the five layers of the scalp. There are also a number of arteries, veins, nerves, and lymphatic vessels that run through those layers. We discuss each of these below.

Arteries of the Scalp

The common carotid arteries, a pair of arteries on either side of the neck, provide the main supply of blood to the scalp. While still in the neck, each of the common carotid arteries splits into an internal and external carotid artery. Each of these branches supplies blood to different areas of the scalp. 

Internal Carotid Artery

The internal carotid artery (on either side of the skull) gives rise to an ophthalmic artery, which further branches into a supratrochlear artery and a supraorbital artery. Both the supratrochlear and supraorbital arteries rise through the supraorbital foramen  (i.e. an opening in the bone just above the eye socket and just beneath the eyebrow) and connect with their counterparts on the opposite side of the skull, as well as with the superficial temporal artery (also on either side of the skull), which provides most of the blood supply to the front of the scalp. 

External Carotid Artery

The external carotid artery (on either side of the skull) branches into the following arteries:

• The superficial temporal artery passes over the back of the cheekbone, where it splits again into a frontal and parietal branch. The frontal branch runs across the temple, supplying blood to the frontal and temporal regions of the scalp. The parietal branch continues over the top of the skull, supplying blood to the parietal region of the scalp. 
• The posterior auricular artery splits away from the external carotid artery just above/behind the jaw and just below the ear. The posterior auricular artery then passes underneath the ear and travels to the deep tissues that converge between the mastoid process (i.e. the protruding, cone-shaped bone found just below and behind the ears on either side of the head) and the cartilage of the ear. This artery supplies blood to the parts of the scalp located above and behind the ears. 
• The occipital artery splits from the external carotid artery at the back of the neck, passing under the ear and in front of the mastoid process. This artery supplies blood to the back of the scalp. 

Veins of the Scalp

The venous drainage of the scalp can be split into superficial and deep components.

Superficial Veins

The superficial veins follow their respective arteries. The supraorbital and supratrochlear veins (on either side of the skull) drain blood from the top of the scalp through the front of the face, while the superficial temporal, occipital, and posterior auricular veins (also on either side of the skull) drain blood from the scalp through the back of the head. Also, just like its arterial counterparts, the superficial temporal vein has a frontal and parietal branch. 

Deep Veins

The deeper regions of the scalp drain into the pterygoid venous plexus (on either side of the skull), which is a large plexus (i.e. a bundle of intersecting blood vessels, nerves, or lymphatic vessels) of veins situated between the temporalis (i.e. thin, fan-shaped muscles on either side of the skull) and lateral pterygoid (i.e. one of the muscles in the jaw that helps us chew) muscles. From there, the venous blood passes into the maxillary vein (on either side of the skull), then into the retromandibular vein (on either side of the skull), and then into the external jugular vein (on either side of the skull), which is the venous counterpart to the external carotid artery. 

The Connection Between Superficial and Deep Veins

It’s also worth noting that there is a drainage connection between the superficial and deep venous systems, whereby parietal emissary veins located in the loose areolar connective tissue layer of the scalp connect to diploic veins that penetrate the skull, eventually flowing into the dural venous sinuses (e.g. superior sagittal sinus) that drain venous blood from inside the cranial cavity. 

Nerves of the Scalp

The front and sides of the scalp are innervated by trigeminal nerves, while the back of the scalp is innervated by cervical nerves.

Trigeminal Nerves

There are two trigeminal nerves – one on each side of the skull. Each trigeminal nerve has three major branches:

• The ophthalmic nerve branches into the frontal nerve, which eventually splits into the following two branches:
• The supratrochlear nerve innervates the front, middle section of the forehead. 
• The supraorbital nerve innervates a large portion of the scalp including the top and sides of the forehead, as well as the vertex. 
• The maxillary nerve branches into the zygomaticotemporal nerve, which innervates the temple.
• The mandibular nerve branches into the auriculotemporal nerve, which innervates the skin in front of and above the ear. 

Cervical Nerves

Cervical nerves emerge from the spinal cord to innervate the rest of the body. There are four cervical nerves that innervate the scalp:

• The lesser occipital nerve (on either side of the skull) arises from the anterior ramus (i.e. front-facing branch) of the second cervical nerve and innervates the skin above and behind the ear. 
• The greater occipital nerve (on either side of the skull) arises from the posterior ramus (i.e. rear-facing branch) of the second cervical nerve and innervates the skin at the upper back of the scalp. 
• The great auricular nerve (on either side of the skull) arises from the anterior rami (i.e. front-facing branches) of the second and third cervical nerves and innervates the skin below and behind the ear. 
• The occipital nerve (on either side of the skull) arises from the posterior ramus  (i.e. rear-facing branch) of the third cervical nerve and innervates the skin at the lower back of the scalp. 

The Scalp’s Lymphatic Vessels

The lymphatic vessels of the scalp are located in the dense connective tissue layer and follow the venous drainage. In general, the front portions of the scalp drain lymphatic fluid through the parotid nodes (i.e. lymph nodes found in front of and just below each ear), which continue to drain through the submandibular lymph nodes (i.e. lymph nodes located just beneath the jaw bone) and deep cervical lymph nodes (i.e. lymph nodes located in the neck). 

The rear portions of the scalp drain lymphatic fluid through the posterior auricular lymph nodes (i.e. a small group of lymph nodes located just beneath the ear) and occipital lymph nodes (i.e. lymph nodes located at the back of the head, near the occipital bone). The posterior auricular lymph nodes drain the area of the scalp located directly behind the ear and flow into the occipital lymph nodes, while the occipital lymph nodes drain lymphatic fluid from the remaining regions in the back of the scalp.

Muscles that Act on the Scalp

There are a handful of muscles that act on the scalp.

The largest and most important muscle in the scalp is the occipitofrontalis muscle. The occipitofrontalis muscle is actually two sections of muscle, known as bellies, that connect to the front and back of the galea aponeurotica. The frontalis belly connects to the galea aponeurotica at the front of the head and inserts into the superior orbicularis oculi (i.e. the muscle that closes the eyelids) near the eyebrow. The occipitalis belly connects to the galea aponeurotica at the back of the head and attaches to the superior nuchal line (i.e. one of four curved ridges on the exterior surface of the occipital bone) and mastoid processes (i.e. the protruding, cone-shaped bones found just below and behind the ears on either side of the head) at the bottom of the scalp. These muscles, or bellies, work in conjunction to pull the scalp back and elevate the eyebrows (the contraction of the frontalis belly creates wrinkles on the forehead). 

The auricular muscles are a group of muscles of the auricle (i.e. the visible portion of the ear). Although there are nine total auricular muscles on either side of the skull, six of those muscles are intrinsic muscles located deep within the skull, while the other three are extrinsic muscles that are located more superficially. It is the three extrinsic muscles that we’re concerned with for this article. 

• The auricularis superior, the largest of the three extrinsic auricular muscles, is a thin, fan-shaped muscle located above the ear. It helps to elevate the ear, attaching to the galea aponeurotica at the top and a tendon just above the ear at the bottom.  
• The auricularis anterior, the smallest of the three extrinsic auricular muscles, is a thin, fan-shaped muscle located in front of the ear. It helps draw the ear upward and forward, attaching to the lateral edge of the galea aponeurotica at one end and cartilage at the top, front of the ear at the other.
• The auricularis posterior is a muscle located behind the ear. It helps pull the ear backward, attaching to the mastoid process (i.e. the protruding, cone-shaped bone found just below and behind the ears on either side of the head) at one end and the lower part of the cranial surface at the back of the ear at the other end. 

Although the auricular muscles play a minor role in fixing the position of the ear, they are considered vestigial in humans. Nevertheless, these muscles may play a role in restricting blood flow to the scalp (more on this in a bit). 

The temporoparietalis muscles are a pair of muscles located just above and in front of the auricularis superior muscles on either side of the head. These muscles lie over both the temporal and occipital bones, connecting to the fascia (i.e. a thin sheath of fibrous tissue enclosing a muscle or other organ) just above the ear on one end and the galea aponeurotica on the other. The temporoparietalis muscles help to fix the galea aponeurotic and elevate the ears. 

The temporalis muscles are broad, fan-shaped muscles located on either side of the head. These muscles cover most of the temporal bones and help produce movements of the mandible, or jawbone, when chewing. Although these muscles are more associated with the mandible than they are the scalp, the contraction of these muscles may restrict blood flow to the scalp, which could have an effect on hair growth/loss (more on this below).

Ways Scalp Mechanics May Impact Hair Growth

Now that you have a better understanding of scalp anatomy, we can examine ways that scalp mechanics may impact hair growth. In particular, the galea aponeurotica and the surrounding musculature may play a role in restricting blood flow (and oxygen) to the scalp. 

We know from previous studies that balding scalps tend to have 2.6 x less subcutaneous blood supply compared to non-badling controls. Moreover, several blood-pressure-lowering medications – such as minoxidil, diaoxide, and pinacidil – have been shown to improve androgenic alopecia – one of the world’s most common hair loss disorders. These findings implicate reduced blood supply as a potential contributor to pattern hair loss. And while it’s still debated just how much the reductions to blood flow are a cause or consequence of androgenic alopecia, there may be a therapeutic benefit to improving blood, oxygen, and nutrient levels to balding hair follicles. 

Below, we examine the impact of scalp musculature on arterial branches, as well as the impact of the galea aponeurotica and surrounding musculature on microcirculation (i.e. capillaries in the scalp).

The Impact of Musculature on Arterial Blood Flow

Dermatologists report that roughly 80% of men with androgenic alopecia tend to have “tight” scalps, suggesting that the muscles around the perimeter of the scalp have involuntarily contracted and are pinching the arterial branches, causing a reduction in blood supply. This is also supported by research measuring scalp hardness in balding versus non-balding men across a variety of scalp regions.^[1]https://www.researchgate.net/publication/338624064_Androgenetic_alopecia_is_associated_with_increased_scalp_hardness

So, do the muscles surrounding the scalp perimeter and anchored to the galea aponeurotica have anything to do with these phenomena? Some evidence suggests yes.

As noted previously, the supraorbital and supratrochlear arteries are two of the three arterial branches that supply the majority of blood to the frontal region of the scalp. These arteries pass through the cranial bone at the eyebrows, run underneath the frontalis muscle, then pierce through the frontalis muscle before running upward toward the hair line. When the frontalis muscle flexes, this flexing can compress the supraorbital and supratrochlear arteries, restricting blood flow to the scalp.^[2]https://academic.oup.com/asj/article-abstract/41/11/NP1599/6206455

In addition, the deep temporal artery resides between the cranium and the temporalis muscles. When these muscles contract, they can compress the deep temporal artery against the skull and constrict blood supply. 

Moreover, some branches of the auricularis anterior and posterior arteries weave between the auricular muscles and their supporting tendons. It is possible that the contraction of the auricular muscles may restrict blood flow in the same manner. 

Finally, while many of the scalp’s arteries reside in the fascia that overlies the scalp muscles, the contraction of the muscles underlying these arterial branches can still affect them. We know this because studies have shown that when the temporalis muscle contracts, the artery overlying it (the superficial temporal artery) constricts by 50%, thus leading to a ~75% decrease in blood supply in that arterial branch.^[3]https://n.neurology.org/content/11/11/935

But that’s not the whole story.

The Impact of the Galea Aponeurotica on Microcirculation

Despite the possible restriction of arterial blood flow described in the previous section, it is generally believed that reductions to blood flow in androgenic alopecia are mainly due to the loss/restriction of the microcapillary networks (i.e., the small blood vessels supporting the hair follicles themselves), rather than reductions from the carotid arterial branches supporting those microcapillary networks.

The microcapillary networks may constrict or compress as a result of mechanical stretch across the galea aponeurotica (mediated by the contraction of the scalp’s perimeter muscles). Because the top of the scalp is a fixed area, stretching of the galea aponeurotica would generate compression of the underlying microcapillary networks supplying hair follicles. 

How Relevant Is Blood Flow to Androgenic Alopecia?

We see hypoxia (i.e. insufficient supply of oxygen) as a trigger of hair loss in mouse models, but is it relevant to humans with androgenic alopecia? Unfortunately, we still don’t know (since there are also reductions to blood supply resulting from the hair follicle miniaturization that follows each re-entry into the anagen stage of the hair cycle). 

Interestingly, there used to be a surgery called “scalp reduction,” where surgeons would place a balloon underneath the galea aponeurotica, slowly inflate it over a series of weeks, and then give patients a surgery to “remove” bald regions and pull the hair-bearing stretched skin over to create the appearance of a fuller head of hair. In the 1990s, these surgeries were quietly abandoned after surgeons started voicing concerns of accelerated hair loss in patients following the procedure. Was this accelerated hair loss caused by skin tension? Did this tension lead to microcapillary compression? We still don’t know the answers, but the questions certainly are interesting.   

Clinical Evidence Suggests Possible New Hair Loss Treatment Targets

Despite the lack of certainty regarding the impact of blood flow (and oxygen) on androgenic alopecia, the results from a number of Botox studies show that when the muscles surrounding the scalp are forcibly relaxed in patients with androgenic alopecia, hair growth/loss improves. 

Botulinum toxin, which is commonly referred to by the brand name Botox, is an injectable neuro modifier that’s used as a therapeutic treatment for many clinical and cosmetic concerns. Specifically, Botox is used to help relax muscles and reduce certain inflammatory signaling proteins. 

Over the last decade, there have been five clinical studies published on the hair-promoting effects of Botox on men with androgenic alopecia. Four of those studies tested intramuscular Botox injections (i.e. injections directly into the scalp’s perimeter muscles), while the fifth study tested intradermal Botox injections (i.e. injections directly into balding regions of the scalp). We examine the results from both types of studies below.

The Results of Studies Testing Intramuscular Botox Injections

Across the four studies testing intramuscular Botox injections, 75-80% of participants responded favorably (i.e. hair growth) with an average hair count increase of 18-21% after 6 to 10 months. Injections into the scalp perimeter muscles were done once every 4-6 months, with results becoming cosmetically significant after the second round of injections. 

In addition to testing the use of Botox injections on their own, one of the four studies also examined using Botox injections alongside oral finasteride (i.e. the active ingredient in Propecia). This combined therapeutic approach led to improved response rates and hair count increases that average nearly 35%. 

Researchers suspect that two mechanisms contributed to these results:

• First, intramuscular Botox injections might relax involuntarily contracted muscles around the perimeter of the scalp. As noted previously, arterial branches run through those perimeter muscles in order to supply the scalp with blood. When perimeter muscles are contracted, they may pinch those arteries, restricting the supply of blood to the scalp. Researchers theorize that injecting those perimeter muscles with Botox helps to unclamp the pinched arterial branches, increasing the supply of blood (and oxygen). 
• Second, by relaxing those perimeter muscles, researchers also speculate that Botox injections might help reduce tension across the top of the scalp, and in doing so, potentially reduce tension-mediated inflammation and/or lower dihydrotestosterone (DHT) in the scalp. 

Despite researcher’s suspicions, it’s important to note that these suggested mechanisms are only speculative at this point. We will need more data in order to corroborate these suspicions. 

The Results of the Study Testing Intradermal Botox Injections

In the one study that tested intradermal Botox injections, 60-80% of participants responded favorably (i.e. hair growth) with an average hair count increase of 5% after 6 months. Injections into balding regions were done every four weeks. 

Although this study’s response rate is similar to the intramuscular studies above, the hair count increases were much lower. It’s worth noting that these results might improve with higher-dose injections. This study used just 30 units of Botox, spread across the entire scalp. When another investigator increased the amount of Botox injected from 30 units to 100 units, and also doubled the frequency of injections, they observed more significant hair growth.^[4]https://www.dovepress.com/getfile.php?fileID=73853  

While conducting the study of intradermal Botox injections, researchers also conducted a cell culture on human hair follicles. They found that Botox appears to decrease the expression of transforming growth factor beta 1 (TGFB-1), a signaling protein that acts as a negative regulator of the hair cycle. TGFB-1 also appears to be intimately tied to hair follicle miniaturization, causing researchers to speculate that intradermal Botox injections might be down regulating TGFB-1 in human hair follicle sites, and in doing so, allowing for hair loss improvements. 

It’s important to note that the reduction of TGFB-1 happens in a dose- and time-dependent manner. Given this fact, it makes sense that increasing both the volume and frequency of intradermal injections evokes a more robust improvement in hair count. 

As with the intramuscular studies above, it’s important to note that the suspected mechanism (i.e. the down regulating of TGFB-1) identified in the intradermal study is only speculative. In order to corroborate this suspicion, more data will need to be collected. 

How Reliable Are the Findings from the Botox Studies?

Although the results from the Botox studies look promising, the amount of evidence on Botox as a treatment for androgenic alopecia is still rather small. And while several research groups have found consistent results, these studies tend to score lower on the hierarchy of evidence. So, we should interpret those results with caution. 

There are at least three significant issues with the Botox studies:

• The Botox Studies Had a Small Number of Participants: To date, fewer than 200 participants have tested Botox to treat androgenic alopecia (in a clinical, peer-reviewed setting). For comparison, thousands of participants have tested the use of finasteride for treating androgenic alopecia. 
• None of the Botox Studies Used a Control Group: At this point, no Botox studies have used control groups (i.e. patients who receive a placebo treatment). Using placebo groups is important because they help researchers control for hair count improvements (and losses) due to seasonal hair shedding. 
• None of the Botox Studies Assessed Hair Diameter: While the Botox studies assessed hair count, they did not examine changes to hair diameter. Androgenic alopecia progresses through the process of hair follicle miniaturization, and we can effectively stop androgenic alopecia by reversing this process. Because we don’t know whether Botox has an effect on hair follicle miniaturization, we also don’t know whether Botox is an effective long-term solution for androgenic alopecia. 

In addition to the above three issues, it’s also worth noting that 1) there are currently no established best practices for the use of Botox to treat androgenic alopecia, and 2) Botox treatment can be rather expensive, with intramuscular injections costing $2,400 to $4,000 per year and intradermal injections running $4,800 to $12,000 per year. 

This isn’t to say we should dismiss the evidence in favor of using Botox to treat androgenic alopecia. At the same time, it’s important not to jump to any conclusions regarding the efficacy of using Botox versus other treatment options. 

Final Thoughts

In this article, we’ve shown how the scalp has a rather complex anatomy – including seven regions on the surface of the scalp; five tissue layers; several bones that the scalp attaches to; a number of arteries, veins, nerves, and lymphatic vessels running through the scalp; and a collection of muscles that pull on the scalp. We’ve also discussed ways that scalp mechanics may impact hair growth, and reviewed five studies that suggest Botox injections may improve hair loss by relaxing the muscles around the perimeter of the scalp.   

Although the findings from Botox studies are still preliminary, they have opened up the possibility of new treatment targets for androgenic alopecia. Any relevant treatment targets would need to relax the muscles around the scalp so that 1) arterial branches can deliver an adequate supply of blood (and oxygen) to the scalp, and 2) tension in the galea aponeurotica doesn’t restrict blood flow in the microcapillary networks that feed hair follicles. 

In addition to the results from the Botox studies, there’s mechanistic research to suggest that skin tension in balding regions (generated from the contraction of muscles around the scalp) might have something to do with the arrival of dihydrotestosterone (DHT) and the balding process itself.^[5]https://www.sciencedirect.com/science/article/pii/S0306987717310411

Finally, it’s worth noting that Botox injections are not the only way to relax the muscles around the scalp. Scalp massages may offer a viable, less-expensive method for treating androgenic alopecia that targets the same mechanisms as Botox injections.