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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.

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Applying Topical Finasteride to the Scalp

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

How to Apply Topical Finasteride Spray

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

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

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

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

How to Apply Topical Finasteride Solution

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

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

How to Apply Topical Finasteride Gel

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

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

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

How Long Should Topical Finasteride be left on Scalp?

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

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

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

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

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

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

There are three big takeaways from this chart:

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

Finasteride Absorption Rates

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

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

A certain percentage of topical finasteride will absorb into the dermis. The bloodstream will absorb some of this later. Time-dependent DHT reductions in the bloodstream can be used to “ballpark” how much DHT is likely also being reduced in the scalp. This is because there is more topical finasteride that percutaneously absorbs than systemically absorbs. For lower dosages, the effects we see in the system can be used as signals for what’s happening – at a minimum – in the scalp skin.

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

Optimal Amount of Time

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

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

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

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

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

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

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

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

Most big-brand topical finasteride companies are:

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

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

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

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

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

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

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

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

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

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

Interested in Topical Finasteride?

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

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

Click Here For 15% Off

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

Types of Drug-Induced Hair Loss

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

Telogen Effluvium

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

Anagen Effluvium

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

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

What About Androgenic Alopecia (AGA)?

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

Psychotropic Medications and Hair Loss: The Research

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

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

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

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

The Process

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

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

Antidepressants

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

• Atypical Antidepressants
  • Bupropion (Wellbutrin)

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

Anti-Anxiety Medications

• Benzodiazepines
  • Clonazepam (Klonopin)

• Buspirone
• Antimantic Agents
  • Lithium
  • Valproic Acid

Evaluation Of Evidence Quality

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

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

Antidepressants and Hair Loss

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

SSRIs and Hair Loss

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

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

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

Escitalopram (Lexapro)

2021 Case Study: 

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

2020 Case Report: 

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

2016 Case Study:

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

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

2011 Case Study:

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

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

Fluoxetine (Prozac)

2021 Case Study:

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

2019 Case Study:

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

2018 Case Report: 

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

2004 Case Study:

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

1992 Drug Trial:

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

Paroxetine (Paxil)

2021 Case Report:

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

2006 Case Study:

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

2001 Double-Blind Randomized, Placebo-Controlled Trial: 

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

2000 Case Report:

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

1999 Case Report:

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

Sertraline (Zoloft)

2015 Case Study:

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

2008 Case Study:

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

2006 Literature Review:

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

2005 Case Study:

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

Atypical Antidepressants

Bupropion (Wellbutrin)

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

2018 Research:

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

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

Atypical Antipsychotics

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

Olanzapine (Zyprexa)

2002 Case Report:

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

Quetiapine (Seroquel)

2007 Literature Review:

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

Anti-Anxiety Medications and Hair Loss

Benzodiazepines and Hair Loss

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

Clonazepam (Klonopin)

2009 Case Study:

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

Buspirone

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

2013 Case Report:

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

Antimanic Agents

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

Lithium 

2013 Literature Review:

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

2012 Literature Review:

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

1994 Case Study:

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

1988 Case Study:

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

1984 Literature Review:

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

1983 Case Report:

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

1983 Case Study:

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

1982 Case Report:

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

Valproate/Valproic Acid

2018 Case Study:

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

2018 Literature Review:

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

2017 Research:

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

2017 Research:

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

1996 Literature Review:

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

1992 Case Report:

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

Establishing Cause and Effect 

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

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

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

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

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

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

Are other medications present?

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

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

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

Are other skin conditions present?   

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

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

Is the patient trustworthy?

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

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

Understanding the Mechanisms of Action

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

Melatonin and Hair Cycle Interruption

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

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

Hypothyroidism

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

Dose Dependency

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

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

Women vs Men

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

Multidirectional Relationships

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

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

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

What Can Be Done?

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

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

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

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

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

Summary

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

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

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

Histamine and Hair Loss

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

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

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

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

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

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What Is The Role Of Histamine In Hair Loss?

How Histamine Works

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

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

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

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

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

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

The Histamine-Hair Loss Connection

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

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

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

The Evidence For Histamine Contributing To Hair Loss

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Do Antihistamines Work Against Hair Loss?

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

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

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

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

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

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

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

Their outcomes showed some of the following features:

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

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

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

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

What’s Our Take On The Data?

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

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

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

Based On The Evidence

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

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

What Then Should Be Done?

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

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

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

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

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

Product Recommendations

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

A simple formulation you can make at home includes: 

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

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

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

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

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What is a Mature Hairline?

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

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

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

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

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

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

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

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

At What Age Does Mature Hairline Stop?

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

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

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

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What is a Receding Hairline?

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

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

What Causes a Receding Hairline?

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

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

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

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

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

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

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

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

Mature vs Receding Hairlines

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

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

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

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

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

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

Diagnosing a Receding Hairline

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

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

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

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

How to Prevent Further Receding

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Summary

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

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

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

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

For men with pattern hair loss who want to combat pattern hair loss, the conflicting advice online can be overwhelming, particularly when it comes to finding the best DHT blockers.

After performing a quick Google search on the topic of DHT blockers, one might navigate to this Healthline article. The piece mentions dietary solutions like coconut oil, onions, turmeric, pumpkin seeds, and edamame. 

Numerous extracts are mentioned as well, including green tea, saw palmetto, reishi mushroom, EGCG, propacil, and zinc.

There are also mentions of pharmaceuticals: finasteride, spironolactone, fluridil, ketoconazole, and dutasteride.

What’s effective? What’s dangerous? Could some DHT blockers actually make hair loss worse? 

It’s time to navigate to the facts, not fiction, about DHT blockers. And determine which ones work and which ones don’t. This article outlines 6 DHT blockers, ranked from worst to best.

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But first, what is DHT?

DHT is short for dihydrotestosterone, which is a hormone made from testosterone. It’s also the main hormone implicated in pattern hair loss, one of the world’s most common hair loss disorders.

This article is not going to dive into the nuances of the DHT-pattern hair loss connection. That’s for a later article. 

For now, readers should note that studies have determined:

1. DHT is elevated in balding scalps ^[1]https://www.jdsjournal.com/article/S0923-1811(03)00249-4/fulltext
2. Men who can’t produce DHT never go bald ^[2]https://www.amjmed.com/article/0002-9343(77)90313-8/pdf
3. Human hair follicle dermal papillae cell clusters undergo cell death and miniaturization when exposed to DHT  ^[3]https://www.karger.com/Article/Abstract/95251
4. By reducing DHT levels in the scalp, many men can stop the progression of hair follicle miniaturization, and even regrow hair.^[4]https://www.jaad.org/article/S0190-9622(98)70007-6/fulltext 

Needless to say, if men want to fight pattern hair loss, they should consider lowering DHT. But herein lies the problem: DHT isn’t just a hormone linked to hair loss; it’s also a hormone that is critical for male development. 

Moreover, in adulthood, DHT seems to be protective against high estrogen levels. As such, men who lower their DHT levels will sometimes report side effects, including weak erections, brain fog, and even gynecomastia – the growth of male breast tissue.

That’s why, when picking a DHT blocker, one must weigh power against safety. In other words, for any DHT reducer, hair density tends to increase in tandem with a heightened risk of side effects.

So, for this article, the six DHT reducers mentioned below are ordered from the lowest clinical efficacy and highest safety profile to the highest clinical efficacy and lowest safety profile. 

1 – Saw Palmetto

Saw palmetto, a palm plant grown in the Southeastern U.S. is one of the most popular herbal DHT reducers, and not without reason. In one clinical study lasting two years, saw palmetto was shown to stop pattern hair loss in 90% of men taking the supplement.^[5]https://journals.sagepub.com/doi/pdf/10.1177/039463201202500435 Other studies have shown a bit of regrowth when combining saw palmetto as a supplement and a topical.^[6]https://www.karger.com/Article/FullText/509905

Based on Perfect Hair Health member results, saw palmetto, by itself, isn’t really that effective as a standalone treatment. But it’s better than nothing, and overall, studies show that the supplement is relatively safe – even over five-year time horizons.

For example, a meta-analysis examined 14 randomized, placebo-controlled studies that had reported adverse events, and found that saw palmetto’s risk of side effects was small, comparable to placebo groups.  When events did occur, they were mainly upset stomachs or headaches experienced after taking the supplement on an empty stomach.^[7]https://link.springer.com/article/10.2165%2F00002018-200932080-00003 Better yet, another study saw no concerning changes to bloodwork… with the majority of side effects reported in the placebo group – or in other words, people who weren’t even taking saw palmetto.^[8]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2518869/ Lastly, out of thousands of participants taking saw palmetto, only a small handful have ever reported reductions in libido. This suggests that the risk of sexual side effects is much less than 1%.

Taken together, this puts saw palmetto first on our list of DHT reducers for men. It has relatively low efficacy, but a high safety profile – and it still does something. In other words, it appears very safe and might help to slow down or stop pattern hair loss. But don’t expect any miracles.

Keep the following tips in mind when taking saw palmetto:

• Take 320mg daily. According to the evidence, effective dosages for hair loss seem to range from 200mg – 320mg daily, depending on the extraction method.
• Split dosages. The volatile acids inside saw palmetto have short half-lives. So, it’s probably best to split up that 320mg daily dosage to half in the morning, half at night.
• Combine with ingredients to enhance absorption and efficacy. Specifically, beta-sitosterol, lecithin, inositol, phosphatidylcholine, and perhaps even niacin and biotin.

These recommendations just scratch the surface, especially in terms of which saw palmetto brands to avoid. But that’s for a later article.

2 – Ketoconazole Shampoo

Ketoconazole is an anti-fungal medication. It’s used to treat skin conditions like dandruff, seborrheic dermatitis, and even jock itch. When formulated as a shampoo, there’s some evidence that it can improve hair counts, increase hair diameters, and potentially even lower scalp DHT levels in men – all without impacting hormone levels elsewhere in the body.

In fact, studies show that 2% ketoconazole, when used properly, boasts an 80% response rate with an average hair density increase of around 5%. Again, that’s no miracle, but with just 1-7% of people reporting side effects ranging from scalp itchiness to scalp dryness, ketoconazole can be considered a low cost, low effort, and moderately effective hair loss intervention.

Two quick notes for those who want to try ketoconazole:

• Get the 2% formulation. The 1% variety is available in supermarkets and drug stores, yet this dilution isn’t clinically effective at fighting hair loss. The 2% version is recommended. The product can be purchased without a prescription at NizoralShop.com.
• Use as directed. In most cases, that’s 2-4 times weekly, with a scalp contact time of 5-10 minutes. Failure to do this might result in wasted money and negligible results.

3 – Herbal DHT Reducers 

Saw palmetto isn’t the only natural DHT reducer out there. There are studies showing that in cell cultures, other substances and herbal extracts can inhibit 5-alpha reductase, the enzyme that converts free testosterone into DHT, and in doing so, potentially lower DHT in humans.

Herbal DHT reducers include:

• Astaxanthin
• Azelaic acid
• Reishi mushroom extract
• Lycopene
• Green tea extract
• Beta-sitosterol
• Alpha-linolenic acid
• Zinc
• Curcumin
• Pumpkin seed oil

And the list goes on.

If we combine these all together, can we reduce more DHT than saw palmetto alone and see increased hair growth?

The logic is understandable. However, in biology, taking more of something doesn’t always equate to greater improvements – especially when taking things that all target the same pathway for DHT reduction: 5 alpha-reductase. 

For instance, in one study, taking 3x the daily dose of saw palmetto for one year did not lead to 3x better improvements to an enlarged prostate; It led to the same improvements as a standard 320 mg dose.^[9]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3326341/ 

Similarly, another study showed that mega-dosing saw palmetto and astaxanthin did not reduce blood levels of DHT any better than a small amount of saw palmetto and astaxanthin.^[10]https://jissn.biomedcentral.com/articles/10.1186/s12970-014-0043-x And with this information in mind, when looking at clinical data on supplements like Nutrafol – which combines many natural potential DHT reducers into one pill – the hair regrowth isn’t really any more impressive than what we expect from a typical dose of saw palmetto alone. 

Which begs the question: why mention the combination herbal extracts above both saw palmetto and ketoconazole? 

There’s not a good answer.

All three of these options are similar in efficacy. But for these herbal combinations, where they differ probably isn’t efficacy; it’s safety. 

There are very few long-term studies evaluating the safety profiles of herbal extracts for blocking DHT, particularly at the mega-dosages featured in best-selling DHT blockers on Amazon. 

Adding in all these extra natural DHT-reducing herbs might have some effect, but one must be very selective in going about it. And those diminutive hair gains might not be worth the massively higher costs or the safety risks versus just taking saw palmetto alone.

Now on to pharmaceutical territory.

4 – Topical Finasteride

For men, finasteride is considered the gold standard treatment for pattern hair loss. Studies show that it can stop pattern hair loss in 80-90% of men, increase hair counts by 10%, and thicken miniaturizing hair – which all in, often equates to 20-30% improvements in hair density.^[11]https://www.sciencedirect.com/science/article/pii/S0022202X15529357 The drug does this by inhibiting an enzyme called type II 5 alpha-reductase, thereby lowering DHT levels by 60-70%.

The problem is that oral finasteride reduces DHT everywhere, and not just on the scalp. In other words, it’s a systemic DHT reducer. And it’s this systemic lowering of DHT that some people use as a surrogate to predict a risk of side effects. 

So people often ask: what if we could just localize finasteride’s effects to only the scalp? Well, that’s what topical finasteride attempts to do. It formulates oral finasteride as a topical –  the medication can be applied directly to the scalp and, hopefully, reduce its risks of going systemic. 

So, does this actually work? 

Yes, to a degree. 

Studies suggest that topical finasteride, at a 1% formulation, is “non-inferior” (or equivalent) to 1mg oral finasteride tablets in terms of hair regrowth.^[12]https://pubmed.ncbi.nlm.nih.gov/19172031/ But concentrations as low as 0.005% have been shown to improve hair growth in men with pattern hair loss.^[13]https://www.tandfonline.com/doi/abs/10.3109/09546639709160517 So, what about the systemic absorption part? Well, this is where things get complicated…

There are studies showing that topical finasteride at a 0.25% dilution can reduce scalp DHT by 24-75%, depending on the amount applied. And while larger applications reduce more scalp DHT, they also appear to have systemic effects on DHT. ^[14]https://pubmed.ncbi.nlm.nih.gov/25074865/

This is because finasteride has a dose-dependent logarithmic effect on DHT reduction. In other words, if just a tiny amount of the drug reaches the bloodstream, it can reduce just as much DHT as a dose that is 25 times higher.

That’s important, because depending on the percent of topical finasteride, the body may be exposed to more of the drug than if taking 1mg of finasteride orally. For example, applying 1mL per day of a 0.25% topical finasteride solution translates to the application of roughly 2.5mg of finasteride to the scalp. 

That’s 2.5-fold more finasteride exposure than a daily 1mg oral dose. And again, just 0.2mg of that dose needs to enter the bloodstream to produce the same DHT-reducing effects everywhere as the oral medication.

For these reasons, many clinicians estimate that topical finasteride is roughly as effective as oral finasteride, but that it only reduces the risk of side effects by 30-50% compared to oral finasteride. There might be ways to lower this risk even further by changing the delivery vehicle of topical finasteride; however, it’s best to address that in a separate article.

5 – Oral Finasteride

Compared to topical finasteride, oral finasteride confers unique advantages: it’s easier to use, it affects all hair follicles rather than just the follicles where the topical is applied, and it’s supported by better clinical data. Across hundreds of studies and tens of thousands of participants, finasteride has demonstrated consistently impressive hair growth outcomes and a decent safety profile. 

Better yet, the drug seems much more effective than its herbal alternatives. In one head-to-head study, it demonstrated significantly better hair growth outcomes over two years with finasteride versus saw palmetto. ^[15]https://pubmed.ncbi.nlm.nih.gov/23298508/ It’s this data that firmly cements finasteride as one of the more powerful DHT reducers on our list.

6 – Oral Dutasteride

Those looking for an even greater DHT-reducing effect may want to consider oral dutasteride. This medication is an inhibitor of type I and type II 5-alpha reductase and it’s prescribed off-label for those looking to treat pattern hair loss at the highest level. 

Depending on the dose, dutasteride can reduce DHT levels by up to 95%. This makes it significantly more powerful than finasteride, with short-term studies showing that 0.5 to 2.5 mg of dutasteride regrows hair 2-5 times faster than finasteride, and even leads to more robust increases in hair counts.

Interestingly, this meta-analysis showed that when used as a hair loss treatment, dutasteride’s risk of side effects was actually comparable to finasteride, despite lowering more DHT.^[16]https://www.dovepress.com/getfile.php?fileID=48173 However, the risk of certain side effects – like gynecomastia – increases with dutasteride versus finasteride. 

So, while it’s likely more effective, it also may come with a slightly higher risk of side effects.

Before concluding, there are a few more things worth mentioning.

First, the only scientifically honest way to compare effectiveness and side effect profiles across DHT reducers is to test them within the same study. This is because patient populations, hair counting methodologies, and side effect questionnaires all vary across hair loss studies. That makes crude comparisons across two random studies really hard to do. 

Since a single study comparing all of these DHT reducers does not yet exist, we can’t claim that this analysis is perfect.

Second, it’s important to keep in mind that in the absolutes, every DHT mentioned here is relatively safe. Finasteride and dutasteride are taken by millions of men every day – most of whom report no issues. 

Hair loss sufferers shouldn’t let these relative comparisons scare them away from trying these pharmaceuticals. If someone cannot tolerate a drug, they can always hop off and try something else.

Third, a few DHT reducers were left out: topical dutasteride, RU58841, procapil, and others. This was intentional: these treatments rely too much on experimental data and unpublished clinical trials to accurately gauge efficacy and safety profiles.

These topics will be covered, at length, in future articles.

Viviscal® is one of the most popular hair loss supplements in the world. What sets it apart from its competition? Clinical research. Viviscal has conducted 12+ human studies on its supplement line, all showing that its proprietary blend of marine extracts can improve hair growth in men and women, and with a variety of types of hair loss.

So, does this make Viviscal the go-to supplement for anyone interested in tackling hair loss naturally?

Maybe, maybe not. If there’s anything we’ve learned from other product reviews, it’s that clinical studies on a supplement rarely tell the full story.

More often than not, these studies can be designed to manufacture biased results; those results can create a false sense of hope; that hope can be transmitted to millions through advertising; that advertising won’t usually convey that the results from those clinical studies aren’t applicable to most of the people watching that ad.

That’s why it’s important to look beyond the marketing of a supplement to really see what that data says.

Before purchasing hair loss products, it’s important to examine the company’s products, marketing, and studies to find out whether this supplement is worth the investment. 

Here’s the Perfect Hair Health approach to product reviews:

1. Buy the product. Send the supplement to a third-party laboratory to test for impurities, heavy metals, and pathogenic microbes.
2. Examine the ingredients. Compare the company’s rationale for these ingredients versus what the totality of research says.
3. Read all published clinical studies. Evaluate their methodologies and results, identify areas of bias, and determine if these results align with the claims made in marketing.

The findings are surprising. The hope is that people fighting hair loss can make better decisions as to whether Viviscal is right for them.

Key takeaways

• Product: Supplement
• Effort: Low (once- or twice-daily supplement)
• Expectations: Clinical trials suggest improvement in as little as 3 months, however, Viviscal™ recommends at least 6 months of supplementation to see results.
• Response rate*: According to the clinical trials:
  • Male pattern hair loss: 85%
  • Women with temporary hair loss from stress, poor diet, or menstruation: 75-100%
  • Autoimmune hair loss: 30-90%
• Regrowth rate*: According to the clinical trials:
  • Male pattern hair loss: 0% (i.e., stabilization)
  • Women with temporary hair loss from stress, poor diet, or menstruation: 10% to 32%
  • Autoimmune hair loss: 5% to 85%. (Autoimmune hair loss is known to spontaneously fully reverse, so it’s hard to delineate how much of this is due to Viviscal versus the mysteries of biology.)
• Cost: $39.99/month
• Problems: Results contingent upon lifelong use; some biased methodologies in clinical research; hundreds of negative reviews online – with most seemingly complaining the product wasn’t effective after 3 months of use (despite one study showing a minimum 32% average increase in hair count after 3 months); for a product sold to millions of people, it’s nearly impossible to find clearcut before-and-after photos submitted by their customers.

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*These response and regrowth rates likely do not reflect reality. Response rates and regrowth rates were calculated using Viviscal’s clinical studies. However, many of these studies came with biased methodologies. Normally, adjustments can be made for these biases in estimates. But the difference between clinical research versus customer reviews was so vast in this case, it’s hard finding a middle ground. The fact that so few before-after photos exist in Viviscal’s customer testimonials – after 25+ years of business – should be a telling sign to consumers. 

Ordering experience

• Checkout: 7/10: One-page checkout made the process relatively easy, but coupon popups and the absence of an autofill or PayPal option made form filling a bit more cumbersome than other checkout pages.
• Fulfillment: 9/10: An email receipt was generated instantly upon receipt of the order, and later to announce that the product had shipped.
• Arrival: 8/10: Arrived within 5 days and without issues.

Highlights

Compared to other hair loss supplements, Viviscal has its perks.

1. The company has conducted 12 clinical trials testing Viviscal™ in men and women with many types of hair loss. All of them show positive results.
2. Viviscal’s supplements don’t contain a lot of extraneous ingredients. This is a positive; many hair loss supplements are chock-full of dozens of vitamins and minerals – many of which are harmful if over-consumed.
3. The supplement contains ingredients that may address some underlying causes of hair loss.
4. The supplement passed our product purities testing for heavy metals, pollutants, and pathogenic microbes. In other words, what you see on the label is what you get.

Having said that, when looking more closely at Viviscal’s clinical trials, marketing efforts, and product ingredients, a lot of issues emerged. Here are just a few.

1. For a company that has conducted 12 clinical studies and been in business for 25+ years, there are almost no before-after photos from customers demonstrating clear, discernible improvements.
2. Most of Viviscal’s studies are either unpublished or poorly designed.
   1. At least 33% of their studies were never published in a scholarly journal.
   2. Of the studies that were published, there are glaring typos and selection biases that make the results less impressive than perceived at first glance. For example, many of Viviscal’s studies use participants who are losing their hair temporarily as a result of stress, bad diets, or menstruation-related nutrient deficiencies. These participants are most likely to see hair regrowth from a nutritional supplement and would’ve also likely seen just as impressive hair growth with better stress management and nutritional planning. Moreover, in the developed world, this hair loss from these causes is relatively less common – and it’s also avoidable with simple dietary and lifestyle adjustments. Therefore, it’s disingenuous (and perhaps deceptive) to market the results of these participants to the general population of hair loss sufferers.
3. Viviscal’s genesis story cannot be verified. Viviscal says that their product was developed after a Scandinavian professor observed that the Inuit peoples’ healthy, long-lasting hair was the result of their diets rich in marine foods. This professor allegedly was able to isolate the compounds responsible for the Inuit’s healthy hair, from which Viviscal was born. 

However, none of this is recorded in any of the clinical studies published by Viviscal. Moreover, Viviscal has not responded to our emails requesting the name of the professor. Rather, research actually points to Viviscal being developed from an earlier product targeting to improve aging skin in women.

A full analysis of Viviscal’s company (and supplements) can be found below.

What is Viviscal®?

Viviscal™ is a hair loss supplement endorsed by hundreds of doctors in the U.S. It’s supported by 12 clinical trials and 25 years of research. It goes without saying that Viviscal is the most heavily researched hair loss supplement out there.

Viviscal® Man

What makes Viviscal unique?

There’s one “ingredient” that makes Viviscal unique from all other hair loss supplements: its proprietary blend of shark cartilage and oyster extract powder, known as their AminoMar™ Marine Complex.

According to the company’s FAQ’s:

“The groundbreaking, clinically proven marine complex available exclusively in Viviscal supplements. Derived from key marine protein molecules combined with a blend of Horsetail (Stem) Extract and naturally occurring Silica, it provides essential nutrients needed to promote existing hair growth from within.”

In fact, this proprietary blend (AminoMar™) has been the focus of every clinical study on Viviscal. Its clinical effectiveness is what makes Viviscal so enticing to consumers looking for a natural solution to thinning hair.

Product Offerings

Viviscal™ offers two product lines based on gender.

For women, they offer a Viviscal™ supplement as well as a shampoo, conditioner, and topical. For men, they offer a Viviscal™ supplement (with slightly different ingredients) and a shampoo.

This review focuses exclusively on Viviscal’s supplements. After all, the supplements are the products that have been clinically studied.

Viviscal Hair Growth Supplement – Ingredients

Both Viviscal™ for Women and Viviscal™ for Men contain:

• Vitamin C
• Calcium
• Zinc
• Horsetail extract
• AminoMar™ (Viviscal™’s properietary blend of shark cartilage and oyster extract power).

However, Viviscal™ for Women also contains niacin, iron, biotin, and millet seed whereas Viviscal™ for Men contains flaxseed. Here’s the full list of ingredients.

Viviscal Woman vs. Viviscal Man: product ingredients

Viviscal™ for Women	Viviscal™ for Men
Vitamin C	Vitamin C
Calcium	Calcium
Zinc	Zinc
AminoMar™	AminoMar™
Niacin	Flaxseed
Iron
Biotin
Millet seed

There are also slight differences in the number of ingredients in each of the male and female supplements. Here are the labels.

Viviscal™ for Women

Viviscal™ for Men

How might these ingredients improve hair loss?

Viviscal’s clinical studies focus on their AminoMar™ proprietary blend. But their auxiliary ingredients – like flaxseed, biotin, and iron – may also help with hair growth for certain people, and in different ways.

Below is a list of Viviscal’s key ingredients and the company’s rationale for their inclusion. The team found some of Viviscal’s claims to be nondescript. These claims were compared against what the actual research says.

AminoMar™

What Viviscal® says

“The groundbreaking, clinically proven marine complex available exclusively in Viviscal supplements. Derived from key marine protein molecules combined with a blend of Horsetail (Stem) Extract and naturally occurring Silica, it provides essential nutrients needed to promote existing hair growth from within.”

What the research says

What’s Viviscal’s original rationale for how AminoMar™ might work? 

After all, their website just says that this marine extract, “promote[s] existing hair growth from within.” That’s a bit vague.

Viviscal’s first study (1993) referenced three earlier studies that tested a similar marine extract.^[1]https://pubmed.ncbi.nlm.nih.gov/1286738/ These studies focused on skin health, not hair health. But interestingly, they found that women using this marine extract also reported improvements to their brittle hair, at least in a survey that asked them about brittle hair.

But when we read these three studies, none of them explained or speculated about the ways in which the marine extract worked, either. To quote from the earliest study we could find:

“Although the mode of action of Imedeen® [the marine extract] is unclear, the results of the present study indicate that there are certain agents in the extract which seem to have a repairing effect on degenerated elastic and collagen tissue in the dermis.”^[2]https://www.ncbi.nlm.nih.gov/pubmed/1864451

Again, this is very vague, and very unusual – especially for a scientific journal. But it seems that more recent research papers (i.e., those after 2010) have tried to offer better explanations.

For instance, this 2019 review attributes Viviscal’s hair-promoting effects to the fatty acids, polysaccharides, and cartilage proteins inside the marine proprietary blend.^[3]https://www.karger.com/Article/FullText/492035

Specifically, the reviewers discuss a polysaccharide (i.e., sugar) called glycosaminoglycan. These sugars are found near the “powerhouse” of a hair follicle: the dermal papilla. This is near the hair follicle base, and it’s where a hair connects to its blood supply.

A hair follicle: note where the blood supply connects to its dermal papilla

When a hair follicle is growing, glycosaminoglycan levels surrounding the dermal papilla increase.^[4]https://www.ncbi.nlm.nih.gov/pubmed/1610689 And when a hair sheds, glycosaminoglycan levels in these regions decrease. Thus, one hypothesis is that AminoMar™ increases glycosaminoglycan levels surrounding our hair follicles, and in doing so, helps a hair grow longer and shed less frequently.

There might be some truth to this, too. In clinical studies on AminoMar™, the extract helps elongate our hair growth cycle – shifting more hairs into their growth stages, and fewer hairs into their shedding stages (more on this later).

Flaxseed (Viviscal® for Men)

What Viviscal® says

According to Viviscal, flaxseed extract is included in their male supplement because it contains vitamin E and omega 3 fatty acids, two substances that they say promote hair health.

“Vitamin E helps to nourish your roots and scalp and is found in Flaxseed. Flaxseed is one of the best foods to eat to combat hair loss, or to give your hair an extra boost of nutrients. Omega-3 fatty acid is in this amazing little, yet powerful, nutrient, helping to prevent your hair from drying out and losing its shine.”

What the research says

There is evidence that vitamin E supplementation might improve hair growth. And vitamin E is found inside flaxseed extract. According to NutritionData, one tablespoon of flaxseed oil (i.e., 14 grams) contains 2.4 milligrams of vitamin E, or 12% of our recommended daily intake.^[5]https://nutritiondata.self.com/facts/nut-and-seed-products/3163/2

Unfortunately, Viviscal supplements include just 0.05 grams of flaxseed extract. Adjusting for the size difference, this implies that Viviscal has only a fraction of 1% of our recommended vitamin E intake. Given that the studies on vitamin E for hair growth used supplements containing 667% our recommended daily intake, the amount in Viviscal is negligible, and likely has zero effect on our hair.^[6]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3819075/

As far as omega 3 fatty acids are concerned, this 2015 study showed that omega 3 supplementation (alongside antioxidants like vitamin E) increased hair counts by ~ 5% in women with general thinning. But again, the amount of omega 3 + vitamin E in that study is dozens of times higher than the amount found in Viviscal, so results really cannot be compared.^[7]https://onlinelibrary.wiley.com/doi/abs/10.1111/jocd.12127

The bottom line: in some cases, vitamin E and omega 3 from flaxseed extract might improve hair loss, but probably not in the negligible amounts found in a Viviscal supplement.

Biotin (Viviscal® for Women)

What Viviscal® says

“Also known as Vitamin H, it is a water-soluble Vitamin B complex (Vitamin B7) that helps the body to metabolize carbohydrates, fats and amino acids, which are the building blocks of protein and thus essential in the formation of the hair structure.”

What the research says

Low-grade biotin deficiencies aren’t uncommon in the U.S. In fact, during pregnancy, about 50% of women will develop what’s known as a marginal biotin deficiency. This is when biotin levels drop slightly below what’s considered normal.

Having said that, marginal biotin deficiencies aren’t linked to hair loss. Rather, biotin-related hair loss is only seen in what’s known as a “profound deficiency”. These occur as a result of genetic mutations, chronic alcoholism, chronic antibiotic abuse, and/or a diet that is completely devoid of biotin for years.

So, just how common are partial or profound biotin deficiencies in the developed world?

Incredibly rare. According to worldwide neonatal screening surveys:

“…The incidence of profound biotin deficiency is one in 112271, and the incidence of partial deficiency is one in 129282.”^[8]https://www.ncbi.nlm.nih.gov/books/NBK547751/

In other words, severe biotin deficiencies occurs in less than .001% of people. And again, only severe biotin deficiencies are causally linked to hair loss.

This begs the question: how useful is it to supplement with biotin for hair?

According to some research groups, not very useful at all. In fact, one investigation team has recommended to “reject the practice of supplementing with high doses of biotin for treating hair loss” unless there is a lab-confirmed deficiency, and that the deficiency is severe enough to be of concern.^[9]https://perfecthairhealth.com/nutrient-deficiency-hair-loss/#biotin

Thus, biotin supplementation (even at the 400% recommended daily intake found in Viviscal®) probably won’t be that helpful, at least for the overwhelming majority of people taking the supplement.

Vitamin C and Iron (iron in Viviscal® for Women only)

What Viviscal® says

“[Vitamin C:] A powerful antioxidant that helps to absorb more Iron into the blood, which in turn promotes hair growth. Vitamin C in Viviscal supplements is sourced from the acerola cherry.”

“[Iron:] An essential mineral that has several important roles in the body, Iron helps to make red blood cells, which carry oxygen around to cells in the body, including hair follicles. Thinning hair can be one of the visible symptoms of anemia (Iron deficiency).”

What the research says

Viviscal’s rationale for including both vitamin C and iron center around an effort to enhance iron levels in their customers.

Vitamin C helps to increase iron absorption. This vitamin is included in both Viviscal® Man and Viviscal® Woman. However, supplemental iron is only found inside the female formulation of Viviscal. And this is because, unlike men, women are at a much higher risk of developing low iron (i.e., anemia) as a result of iron loss from menstruation.

There’s some evidence to support these positions. For instance, studies have linked mild-to-severe iron deficiencies in women to a variety of hair loss disorders – ranging from female pattern hair loss to telogen effluvium.^[10]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3678013/ ^[11]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6385517/ And while there’s still debate over how effective (and how high) iron levels need to raise in order to improve hair loss, it goes without saying that a lot of women have experienced great improvements to hair growth by restoring their iron to adequate levels.

Unfortunately, supplemental iron also harbors some risks. This is because iron is oxidative – meaning that in excess, its presence can create oxidative stress, also known as inflammation.

In fact, evidence indicates that vitamin C and iron salts (like the ferrous fumarate used in Viviscal™ for Women) may have a dangerous and synergistic interaction. Specifically, research suggests that vitamin C can “propel” the oxidative action of iron, meaning that vitamin C may enhance the inflammation that excess iron causes.^[12]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC340385/ This suggests that in cases of longterm, excessive iron + vitamin C supplementation, we’re more likely to experience problems like ulcerations, inflammation, exacerbation of chronic disease, and, potentially even cancer.

Customer testimonials

It’s one thing to look at a supplement’s ingredients, then build a case for whether the research shows these ingredients will or won’t help with hair loss. It’s another thing to measure whether all of these ingredients – when taken together – actually improve hair growth in men and women with thinning hair.

To do this, one can analyze two pieces of evidence:

1. Customer testimonials. Viviscal has been in business for 25+ years. They claim to average one product sale every single minute of the day. That equates to millions of customers, and (hopefully) thousands of before-after photos.
2. Clinical research. Viviscal is the most heavily studied hair loss supplement in the world. If Viviscal’s clinical research proves as promising as claimed in their marketing, then customer testimonials should be validated in the data: increases to hair counts, hair diameters, etc.

This section focuses on that first lever: customer testimonials and before-after photos.

12 clinical studies and 25+ years of business. But where are the before-and-after photos?

When it comes to hair loss, before-and-after photosets are probably the most powerful tool used to validate the effectiveness of any approach. Yes, clinical trials are great (and often required). As will be discussed later, clinical research is only valid when a study is properly designed. Thus, if a product truly works, one can expect to see a combination of both clinical evidence + customer testimonials.

On review websites, customer reviews of Viviscal are mostly negative. However, these reviews were left out of this product review. Why? Because reviews can be written by anyone – including competitors or Viviscal employees. And given the inability for review websites to verify and rank the validity of any review, the focus remained on hard evidence: that of which is presented by Viviscal on their own website.

So, as one of the best-selling hair loss supplements on the planet, how does Viviscal do in the customer success department?

Puzzlingly, Viviscal has almost no customer before-and-after photos (at least on their website).

And of the ones that are featured, it’s as if they’re designed to be intentionally misleading. These can be segmented segment this by the photos featured on Viviscal’s (1) main website, (2) female site, and (3) male site.

The photos featured on Viviscal® appear to have had their backgrounds trimmed and/or recolored. This masks any lighting differences across photos; it makes fair photo comparisons impossible.

The success featured on Viviscal® Woman aren’t actually focused on hair; rather, they’re simply photos of women wearing different hairstyles before and after starting the supplement.

And the few customer photos featured on Viviscal® Man either face the same problems above or were taken from impossible-to-compare angles and lightings.

Why is this concerning?

Well, in their marketing, Viviscal claims that one packet of Viviscal is sold every single minute. This should equate to 10+ million customers over a 25-year period. And if the product were truly as effective as advertised, one would expect Viviscal to present significantly more before after-photos, and of significantly better quality.

For instance, let’s assume that Viviscal only has one million consistent customers (a fraction of what is suggested in their marketing). Now assume that just 0.1% of those customers (or one in 1,000) decide to take before-after photos, then share those photos with Viviscal. That leaves Viviscal with 1,000 before-after photos from which to share on their website.

For some reason, Viviscal seems to only have ~20 photosets total across men and women. And instead of high-quality photo comparisons, we’re left with misleading photosets.

What about before-after photos from Viviscal’s clinical studies?

It’s true that Viviscal’s clinical studies have higher-quality photosets, and that in some cases, these photosets demonstrate clear, discernible hair regrowth. But it’s also important to contextualize these photosets – because not all photos are from people with common hair loss types.

For men with androgenic alopecia (AGA) – the most common form of hair loss in adult men – the highest-quality before-after photoset available from a Viviscal study only showed stabilization after 180 days of use. In fact, this is the one advertised on their website.

For women, the highest-quality before-after photosets come from their website (here) and clinical studies ^[13]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509882/

But these women only had temporary forms of hair loss due to stress, poor diet, and nutrient deficiencies due to menstruation. In other words, these before-after photos don’t represent what the average Viviscal customer should expect, because hair loss from these causes are lesser common, and likely do not represent the average customer of Viviscal.

 Now for Viviscal’s clinical studies …

Clinical studies

When it comes to clinical studies on a hair loss supplement line, Viviscal® is the industry leader.

According to their marketing materials, Viviscal has conducted 12 clinical trials – more human studies on their product than any other hair loss supplement out there.

And even better, these clinical trials aren’t limited to just one population, or one type of hair loss. Of the 12 clinical trials, seven were conducted on women, two were done men with androgenic alopecia (AGA), and two were completed on men and women with autoimmune hair loss disorders like alopecia areata, alopecia totalis, and alopecia universalis.

In other words, they’ve not only got the most clinical studies, but they’ve also studied their supplement on the majority of types of hair loss out there. And amazingly, all of the studies have appeared to reap great results.

Viviscal’s clinical studies: summarized

Viviscal™’s Clinical Trials, Their Subjects, and the Results
Study #1 (2014)	Females with Self-Perceived Hair Thinning	“• 32% increase in terminal hairs after 3 months • 39% decrease in hair shedding • After 3 months there was significant self-perceived improvements in overall hair volume, scalp coverage and hair strength.”
Study #2 (2014)	Females with Self-Perceived Hair Thinning	• 57% increase in terminal hairs after 3 months • 80% increase in terminal hairs • 12% increase in hair diameter after 6 months • After 3 and 6 months there was a significant self-perceived improvement in overall hair volume, scalp coverage, hair and nail strength.
Study #3 (2014)	Females with Subclinical Hair Thinning	“• a 7.4% increase in hair diameter after 6 months • an 18% reduction in hair shedding after 3 months.”
Study #4 (2014)	Females with Self-Perceived Hair Thinning	• 94% in hair volume • 92% hair thickness • 91% in nail growth rate and • 92% in nail strength After 6 months.
Study #5 (2012)	Females with Self-Perceived Hair Thinning	• 111% increase in terminal hairs after 3 months versus no change amongst the placebo subjects. • 125% increase in terminal hairs after 6 months versus no change amongst the placebo subjects. • After 3 and 6 months there were significant self-perceived improvements in overall hair volume, thickness, and scalp coverage.
Study #6 (2011)	African American Females with Self-Perceived Hair Thinning	“Rapid changes in hair growth and appearance in as little as 2 months.”
Study #7 (2010)	Females with Self-Perceived Hair Thinning	“After a 10 week period, there was an average 46% reduction in hair loss reported. 75% saw an increased thickness in the body of their hair and 75% saw an increase in overall hair volume.”
Study #8 (1997)	Men with AGA	• 75.3% of patients observed a significant decrease in hair loss • 14.6% of patients showed partial regrowth
Study #9 (1996)	Males and Females with Alopecia Areata, Alopecia Totalis, or Alopecia Universalis	• 92% of areata group showed regrowth of permanent hair. After four months of treatment: • 83.3% of totalis group showed regrowth of permanent hair and • 31.8% of universalis group showed regrowth of permanent hair after five months. • Complete cure was observed in 14% of areata, 25% of totalis and 5% of universalis.
Study #10 (1994)	Men with AGA	“Hair loss stopped for 100% of subjects after two months treatment. 43% showed total regrowth, 23% showed three quarter regrowth, 13% showed half regrowth & 13% showed 30-50% regrowth.”
Study #11 (1992)	Men with AGA	“100% of treated subjects reported that hair loss had stopped after 2 months of treatment. Mean increase in non-vellus hair of 38% was recorded in patients after 6 months treatment. 95% of subjects showed both clinical and histological cure.”
Study #12 (1992)	Males and Females with Alopecia Areata, Alopecia Totalis, or Alopecia Universalis	“85% of subjects with Alopecia Areata were completely cured & 10% showed significant improvement. 25% of subjects with Alopecia Totalis were completely cured & 20% showed significant improvement.”

At a glance, this body of clinical research seems to position Viviscal as the go-to supplement for anyone with thinning hair. But as the Perfect Health team learned from its investigation into Nutrafol, clinical trial results can be misleading.

For instance, studies can pick participants who most likely have nutrient deficiency-related hair loss, and are thereby most likely to see hair regrowth from taking any nutritional supplement (not just the brand being investigated. Studies can also use biased hair counting methodologies to make it appear as though a supplement regrows a ton of hair, even when the results don’t translate to visual improvements to hair density.

So, do Viviscal’s studies have any of these biases?

In many cases, yes.

Whether or not these biases invalidate the body of research of Viviscal remains to be seen. It would be unproductive to go through each Viviscal study and dissect every little problem. Doing this would turn this already-long product review into a full-fledged novel.

In focusing more on the larger issues across these studies, hair loss sufferers can decide for themselves whether these concerns are worrying enough to influence purchasing decisions.

Problem #1: at least 33% of Viviscal’s clinical trials were never published

It’s one thing to conduct a clinical trial, analyze the data, write the results into a manuscript, submit that manuscript to a journal, get it reviewed by experts, receive feedback, make revisions, resubmit, and then finally have your study accepted for publication in a scholarly journal.

It’s another thing to conduct a clinical trial, analyze the data, write the results into a manuscript, and then bypass peer review and, instead, just publish the results as part of your marketing materials.

According to Perfect Hair Health research, 33% of Viviscal’s clinical trials fall under that secondary category. Of the 12 studies listed on Viviscal’s website, our investigation showed that four studies (#4, #6, #7, and #12) never made it into a scholarly journal. In fact, 3 of those 4 studies were never even submitted for publication.

Why not publish the results of a clinical trial in a scholarly journal, especially if the results are positive?

This is actually more commonplace than most people realize. In fact, conducting a clinical trial and not publishing the results in a scholarly journal happens all the time – especially for companies studying (and selling) natural health products.

Just take the companies selling low-level laser therapy devices. Companies in that hair loss sector have a history of registering clinical trials containing biased hair counting methods (e.g.., grouping vellus + terminal hair counts). These companies never intend to submit their results to a scholarly journal. Rather, they conduct these studies so that when their great (manufactured) results come in, they can legally claim their devices can “increase hair thickness by over 200%”.

In these cases, the goal isn’t to prove that the clinical research is legitimate; the goal is to avoid getting sued over false claims.

As such, it’s not a priority for these companies to submit their clinical data for peer review. If they did, reviewers would likely find the flaws in the study design, and then reject the study for publication.

Therefore, the most common reason why a company won’t publish clinical results in a journal – at least when those results are favorable – is that they know that the study is biased, and that the paper won’t survive peer review. So, instead, these companies will just write up their results to look like a paper, and then use it as part of their marketing.

(Note: this is different from burying unfavorable clinical trial results – or in other words, never publicizing the findings. This is what Nutrafol is suspected of doing for one of the clinical trials that they completed, but never published.)

For Viviscal, favorable unpublished clinical trial results make up 33% of the studies advertised on their website.

Now, this isn’t the end of the world… because that still leaves 8+ studies that have gone through peer review, and have been published in journals.

So, how do these published trials stack up?

Well, these published studies also have issues. This leads to another problem.

Problem #2: of Viviscal’s published studies, most of them were published in low-ranking journals

Low-ranking journals, and why they should be avoided

If the four studies Viviscal never published were ignored in favor of the eight studies that survived peer review, there would still be a great deal of noise that makes Viviscal’s emphasis on their clinical research problematic.

For starters, these eight clinical studies weren’t published in high-ranking dermatology journals. Rather, they were published in lower-ranking journals in dermatology and medicine. These are journals that rank below the top quartile, according to SciMago Journal Rankings.

Now, one might wonder, “Who cares about a journal’s ranking? Peer review means peer review!” But unfortunately, this isn’t true. This is because not all peer review is created equal.

Quality reviewers – those of reputable institutions and research centers – generally reject review requests from unknown or lesser-respected journals. Why? Because the papers submitted there are often of lower quality. This forces lower-quality journals to send mass emails of review requests –until they either find someone to accept the review or they decide to make a decision on the paper without any external review at all.

In the case of low-ranking journals, too often are their reviewers people with zero expertise regarding the manuscript in which they’re reviewing.

For example, Perfect Hair Health has published two papers about androgenic alopecia. A list of the last three review requests from low-ranking journals? Manuscripts about:

• Dapsone-loaded micro sponge gel for acne management
• Business management practices
• R&D teams: how innovation and performance varies between large American and Chinese firms

All three review requests were declined because the company only publishes research on hair.

So, just think of how far down a list someone has to get before they contact Perfect Hair Health: someone with zero experience, let alone expertise, in any of these fields.

What’s worse: a quick Google search just revealed that two of these three papers passed peer review, made it into a journal, and are now indexed in scholarly databases. That suggests they were reviewed by someone! If not me, then who? Someone with an equally absent level of expertise? Or nobody at all – given some journals’ incentives to collect authors’ payments in exchange for publications?

Now, back to Viviscal.

The company did, in fact, publish their clinical studies in lower-ranking journals. Knowing this, is there evidence that these studies weren’t properly reviewed?

Yes. In fact, one can identify – just by reading these papers – errors so big, they should’ve been flagged by literally anyone reading the paper.

Example 1: grammatical errors… in the first sentence of a paper

See the first of Viviscal’s 2015 study, published in International Journal of Trichology:

“Since skin and hair quality are potent vitality signals, and hair growth deficiency can cause significant psychological morbidity.”

That’s not even a complete sentence.

Example 2: hair count increases of 1,381%

In Viviscal’s first-ever study, investigators show the results of Viviscal supplementation on hair counts of men with androgenic alopecia (AGA) after six months. Their final hair count increase? A jump from 1,238 to 17,101 hairs per measured region… an increase of 1,381%.

Obviously, this is just a typo. The investigators clearly meant to write 1,710 and not 17,1010 (as indicated by the hair count differences listed in the final row). But a serious reviewer should’ve caught this.

This is the difference between publishing in reputable journals, and publishing just so you can tell people that your product has a peer-reviewed clinical study. The former actually matters; the latter is just for marketing.

Problem #3: Many of Viviscal’s studies have selection bias. Many were done on people with a type of hair loss that doesn’t represent the majority of Viviscal consumers.

It doesn’t just matter how people write up a clinical study; it also matters how that study was conducted. And in this regard, many of Viviscal’s published studies have serious problems. This is especially true in the way that they’ve selected participants for their study.

For reference, there are dozens of types of hair loss, and each type has a different set of causes. The most common types of hair loss are (1) androgenic alopecia (AGA) – also known as male and female pattern hair loss, and (2) telogen effluvium.

Current census is that AGA is caused by a combination of hormones and genetics. It’s chronic, progressive, and without treatment, it worsens. Conversely, telogen effluvium is a form of temporary hair loss. It’s got a wide set of causes – stress, medication use, hypothyroidism, etc. – and once the underlying cause of telogen effluvium is resolved, usually the hair will return in 3-6 months.

For women, one common cause of telogen effluvium is a nutrient deficiency. And one of the most common nutrient deficiencies in women of “childrearing age” is iron – because women lose iron each month during menstruation.

Therefore, this is a percentage of women losing their hair from telogen effluvium – a temporary form of hair loss. And a percentage of those women have telogen effluvium due to low iron stores. If these women correct their low iron stores, they’ll often regrow their hair.

So, let’s look at some of the best Viviscal studies: the ones published in journals that are lower-ranking, but still high enough to likely find reputable reviewers.

These studies were conducted in the U.S. That means they had to register the trials on clinicaltrials.gov. And whenever a trial registers on this site, they have to outline the selection criteria for participants. In other words, they have to tell you how the investigators selected people to include (or exclude) as part of their study.

So, when it comes to participant selection, what do all three of Viviscal’s US-based clinical trials have in common?

All of the studies selected women with temporary forms of hair thinning – mainly the result of poor diets, stress, or menstrual cycles – of which would’ve resolved without a nutritional supplement if the person had just taken measures to get more of those nutrients into their diets.

To quote directly from the trial setups:

 “Inclusion Criteria: Females with self-perceived thinning hair associated with poor diet, stress, hormone influences or abnormal menstrual cycle.”

All of these clinical trials showed statistically significant hair count increases to Viviscal after 3-6 months of use. Not surprisingly, at least two of these trials were conducted by the Ablon Group – the research institution that used nearly the same selection criteria for Nutrafol’s clinical study – which sufferers from the same problems will be illustrated.

Why is this such a problem?

For two reasons.

Firstly, this selection criteria is incredibly narrow. Women with telogen effluvium from a nutrient deficiency represent only a fraction of people with hair loss. While there’s no data on the incidence of nutrient deficiency-driven telogen effluvium, it probably responsible for less than 10% of hair loss cases in the U.S.

This means that if Viviscal advertises its “clinical results” to all U.S. hair loss sufferers – the results from their clinical trial won’t apply to 90% of them. But consumers don’t know this. They read the words “clinically proven”, and expect that this product applies to them and will reap positive results.

That’s the first problem.

The second problem is that if the women in this study had just reduced their stress levels, improved their diets, and/or made an effort to get more iron, they likely would’ve seen the same degree of hair regrowth… and without the aid of a supplement that costs $39.99 every month.

After all, studies on women with nutrient deficiency-related telogen effluvium have shown equivalent increases in hair counts – without Viviscal’s proprietary ingredients – and all with a basic nutritional supplement.^[14]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6136400/

Are there any studies that fairly assess Viviscal?

Yes.

There is one clinical study on Viviscal that appears to meet this criteria. It was done on men with androgenic alopecia (AGA) – the most common cause of hair thinning for adult males.

It was a 1997 study conducted on 200 men with AGA, all of whom were instructed to take Viviscal® for Men twice daily for six months. The study wasn’t published in a high-ranking journal, but it also didn’t have the same selection criteria biases identified in Viviscal’s more recent studies.

Moreover, the study had clearly defined methodologies. The researchers used objective measurements for results – like hair count changes using a trichogram, or hairline changes by calculating the distance between the hairline and the eyebrows before and after treatment. In addition, the researchers also had participants complete a self-assessment survey to standardize their opinions of the supplement.

Over the six-month period, 32 men dropped out of the study. But of the 178 men who completed the trial, here were their results:

• Across all Viviscal users, hair counts increased by 4% (statistically insignificant)
• 75% of men reported a decrease in hair loss (i.e., the rate of hair loss slowed)
• 15% of men showed partial hair density improvements

These results aren’t that impressive. But, in our opinion, they’re the fairest results ever published on Viviscal. Why? Because they set realistic expectations of the supplement.

Males with AGA who are taking Viviscal should set their expectations that the supplement simply slows down the progression of hair loss; the supplement will not fix the problem. And for those who (1) are happy with that expectation, (2) understand the effects only last with continued use, and (3) don’t mind paying $39.99 per month indefinitely – then this supplement might be a good choice.

Viviscal’s clinical research: the bottom line

• Viviscal boasts over 12 clinical studies on their product line – more studies than any other hair loss supplement.
• However, of these 12 studies, four of them were never published in a scholarly journal.
• Of the studies that were published, these clinical trials were published in low-ranking journals that tend to have really easy peer-review procedures,
• Resultantly, these studies were published with problems that would’ve been flagged – and likely would’ve led to a rejection – in reputable journals: for example, typos in the opening sentences and selection biases for participants.
• This is most evident with three of Viviscal’s published studies: the ones that tested the supplement on women with temporary hair thinning as a result of stress, a poor diet, or menstruation-related iron loss. These types of hair loss sufferers are most likely to benefit from a basic nutritional supplement – particularly ones containing iron, zinc, and antioxidants.
• Moreover, hair loss due to a nutrient deficiency is relatively uncommon compared to all hair loss causes. This type of hair loss accounts for just a small fraction of hair loss cases in the U.S. – likely less than 10%. Therefore, it’s unethical to advertise these results as “clinically effective” to all people with hair loss, when the results only apply to a small portion of a people hearing the claim.
• There is one study on Viviscal that seems fairly conducted: a trial on 200 men with androgenic alopecia (AGA). This is the most common form of hair loss in adult men. The trial found that Viviscal did not statistically improve hair counts, but that the supplement did help decrease the rate of hair loss for these men.

As such, our takeaways on Viviscal’s clinical research are the following:

1. The product is great for females with hair loss due to a poor diet and/or nutrient loss from menstruation.
2. The product is great for males with AGA who want to take a natural approach to improving their hair and only want to slow down the rate of hair loss – and are comfortable spending $39.99 per month to do so.

Otherwise, we think that Viviscal by itself is not an effective solution for most people with hair loss, and that this money could be better invested elsewhere.

Product purity: heavy metals, microbes, and contaminants

While Viviscal’s clinical studies and testimonials aren’t as impressive as they look at first glance, there is good news. The company makes a high-quality supplement… at least in terms of product purity.

The Perfect Hair Health team bought Viviscal® For Men and sent it to a third-party lab testing facility to test for contaminants often found in consumer supplement products: heavy metals, pathogenic microbes, and impurities related to materials processing.

There were no red flags. By all means, this supplement appears to be made well. What you see on the ingredients list is what you get.

Viviscal® Man purity: heavy metals, microbes, and pesticide residues

This is a positive, as some products that the Perfect Hair Health team has reviewed (i.e., Hairguard Anti-Hair Loss Essentials Supplement) have demonstrated an absence of the ingredients they list on their product labels.

BONUS: How did Viviscal start?

This isn’t related to our analysis of the supplement, but it’s a part of our investigation worth sharing.

Viviscal says that the company all began with the discovery (and development) of AminoMar™ Marine Complex – a proprietary blend of shark cartilage and oyster extract power. According to their website:

“AminoMar is a proprietary marine complex available exclusively in Viviscal hair growth* supplements. In the 1980s, a professor from Scandinavia discovered that the Inuits’ great hair and skin was the result of their fish- and protein-rich diet. He isolated the key protein molecules in their diet and it was from these origins that AminoMar was created. Since then, Viviscal has been tried and tested by clinicians around the world.”

The story sounds almost too good to be true. An unnamed Scandinavian researcher… An observation made amongst the Inuits…. The identification of diet as responsible for the Inuit’s great hair… The isolation of key protein molecules from that diet… The packaging of these molecules into a clinically supported supplement.

Is there any validity to this story?  The Perfect Hair Health team attempted to identify this mysterious Scandinavian researcher, his early research on the Inuits, and how this research eventually culminated into the product Viviscal.

These efforts just led to more confusion.

Viviscal’s beginnings: fact or fiction?

Research began by combing through Viviscal’s earliest published studies from the 1990s. It was assumed that in these early papers, Viviscal would discuss their novel proprietary blend: how they came across it, how the blend’s suspected effects might improve hair growth, and why the company has decided to study the blend in a clinical setting.

Unfortunately, the team couldn’t find any references mentioning the story that Viviscal explains in their marketing.

The closest thing identified was a 2019 literature review on alternative hair loss treatments, “Complementary and Alternative Treatments for Alopecia: A Comprehensive Review.” According to that review:

“Marine proteins, including extracellular matrix components from sharks and mollusks, have been produced for over 15 years to enhance hair growth. A Scandinavian researcher first described the exceptionally healthy skin and hair of the Inuit peoples to be a result of their fish- and protein-rich diet [36, 37]”.^[15]https://www.karger.com/Article/FullText/492035

But when checking the review’s references (i.e., studies “[36, 37]”), it was found that those studies didn’t actually support the claims made in that quote.

For instance, that first reference is to Viviscal’s first-ever study.^[16]https://www.ncbi.nlm.nih.gov/pubmed/1286738 That study had already been read and there was no mention of Inuits or a Scandinavian researcher. The second reference (i.e., “37”) couldn’t be found either. Why? Because according to Viviscal, that reference is to a clinical trial that was never even published.

So, the digging continued. The only thing to do next: read all of the studies mentioned in Viviscal’s first study from 1992. In other words, read the papers within a paper.

Still no references to a Scandinavian researcher or the Inuit… or anything about how this marine extract was developed or its purported mechanisms of action.

A how-to guide on passing peer review

The closest thing the team could find were studies on a product called Imedeen® – a marine extract supplement that was shown to improve skin health in females. These studies were done from 1991-1992 – one year before Viviscal’s first study – but these studies also don’t mention what prompted anyone to start studying these marine extracts.

What is Viviscal’s true genesis story?

This remains unknown. Perfect Hair Health reached to Viviscal® in a good faith effort to obtain the name of this Scandinavian professor, so that the team could verify the story they tell in their marketing. No reply has been recieved.

Interestingly, a 2001 clinical study on HairGain® – the earlier brand name of Viviscal® – was found.^[17]https://www.researchgate.net/publication/12056799 This study showed that the supplement led to impressive hair regrowth in men with androgenic alopecia. The study was done by a man named Erling Thom – a Scandinavian researcher who was later accused of falsifying data in the studies he conducted on alternative health products.

The team couldn’t find any evidence tying Erlin Thom to Viviscal’s earlier clinical research. But there also wasn’t any evidence that he wasn’t involved. After all, Viviscal’s elusive genesis story seems to have no paper trail – which is odd for a product involved in so much clinical research.

It appears as though Viviscal was created from Imedeen® – an earlier product that contained a similar marine extract, but was positioned for improving aging skin rather than hair loss. Survey portions of Imedeen® studies in the early 1990’s showed that women also reported improvements to their brittle hair. So, our guess is that marketers of Imedeen® saw an opportunity to retarget the product, and either sold off or repositioned the marine extract into a hair supplement and later started testing it on hair loss sufferers.

But as far as this Scandinavian professor, his observations on the Inuits, and the actual identification of why these marine extracts might prove helpful to skin or hair… this part of the story seems to remain lost in time (and clinical research).

Viviscal®: who are the best candidates?

Viviscal® might be right for …

• Females with hair loss due to a poor diet and/or nutrient loss from menstruation.
• Males with AGA who want to take a natural approach to improving their hair and only want to slow down the rate at which they’re losing hair – and are comfortable spending $39.99 per month to do so.

Viviscal® might not be a good fit for …

• Male with AGA with expectations any higher than the above.
• Females with hair loss related to thyroid dysfunction, PCOS, childbirth, stress, vitamin D deficiency… or virtually anything else outside of the nutrient deficiencies that Viviscal® Woman helps to address (i.e., fatty acids, iron, and zinc).

The bottom line

Viviscal is the most clinically studied hair loss supplement on the planet. But that doesn’t mean it’s the best hair loss supplement available. This is obvious at the outset with Viviscal’s relatively low number of customer before-after photos featured on their website – which, for a company with millions of customers over 25+ years, is a little unusual.

Moreover, Viviscal’s clinical research isn’t as impressive as conveyed in its marketing. For starters, at least 33% of their clinical studies were never published in a scholarly journal. Of the ones that were published, all of them were published in low-ranking dermatology journals – with many of those studies containing glaring typos and selection biases that would’ve led to their rejection from reputable journals.

In addition, the Viviscal studies producing the clearest before-after photos were done on women with temporary hair loss due to stress, a poor diet, and/or nutrient deficiencies as a result of menstruation. This specific type of hair loss is the one that is best positioned to respond to a nutritional supplement, and it’s also a type of hair loss that is (1) relatively uncommon among hair loss sufferers in the developed world, and (2) one that can be improved without a $39.99 supplement – and just through lifestyle and dietary changes.

Lastly, Viviscal®’s genesis story of a Scandinavian professor – his observations on Inuits, their hair-healthy diets, and the isolation of marine compounds responsible for the Inuit’s great hair – is either exaggerated or fabricated. After review, it can be assumed that this product was developed from an earlier skincare product (with a similar marine extract) after survey research found that women thought that product also improved their brittle hair.

On the positives – Viviscal® Man did pass Perfect Hair Health’s third-party laboratory testing for heavy metals, pollutants, and pathogenic microorganisms. In other words, what you see on the label is what you get. But unfortunately, this isn’t enough to earn a recommendation – especially given its price point and the discrepancies in Viviscal’s real-world results versus their clinical research.

Questions? Comments? Please reach out in the dedicated forum thread below

Anyone searching “How to reverse hair loss online” has undoubtedly come across the Big Three protocol: minoxidil (Rogaine®), finasteride (Propecia®), and ketoconazole shampoo (Nizoral®).

What many might not know: despite ketoconazole’s popularity, it’s not actually FDA-approved for pattern hair loss, nor is it as well-researched as minoxidil or finasteride.

In fact, there are just a few human studies on Nizoral for hair loss and even fewer on people with just androgenic alopecia, the most common form of hair thinning in men.

Interested in Topical Finasteride?

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

Is Ketoconazole Worthy of Big Three Status?

Here we’ll uncover the evidence on ketoconazole for hair regrowth. We’ll cut straight-to-the-facts about ketoconazole, its effects on hair loss, and whether or not this shampoo is a good fit. Along the way, we”ll also uncover…

• Which formulation is better: 1% or 2% ketoconazole
• Why not everyone is a good candidate for ketoconazole
• How to (potentially) increase ketoconazole’s efficacy (see our before-after photos)
• Who needs to worry about ketoconazole’s potential side effects

Nizoral for Hair Loss: Overview

• Effort: Low (used as shampoo just 2-3 times per week)
• Expectations: According to studies so far, hair loss improvement is observed after 3-6 months
• Response rate: 80%+
• Regrowth rate: ~5% alone; 25-40% if combined with microneedling and/or finasteride and/or minoxidil
• Cost: Low ($10-$20 per bottle of 100ml, which should last two months)
• Problems: Not as well-studied as finasteride or minoxidil; 2% formulations work better but generally require a prescription (though this can be circumvented online); less studied on women (though it’s likely just as effective)

Key Takeaways

Ketoconazole is a low-cost, low-effort shampoo with practically no side effects. It’s clinically shown to help improve hair loss from both androgenic alopecia (AGA) and telogen effluvium (TE).

While 1% ketoconazole is available over the counter, 2% ketoconazole usually requires a doctor’s prescription. Studies show that 2% ketoconazole is more effective, particularly in helping to normalize excessive hair shedding from rapid-onset AGA and/or TE. ^[1]https://pubmed.ncbi.nlm.nih.gov/9669136/

Can Nizoral help with hair growth?

If a 2% prescription-strength formulation is used, yes.

By itself, ketoconazole is unlikely to stimulate hair regrowth on par with finasteride or combination therapies. So, ketoconazole is just one part of a multi-pronged hair loss regimen. This shampoo may have synergistic effects with stimulation-based therapies like microneedling, massaging, and/or platelet-rich plasma therapy. It also seems to pair well with most FDA-approved / FDA-cleared treatments like finasteride, minoxidil, and low-level laser therapy.

While oral ketoconazole comes with significant risks of side effects, 2% ketoconazole shampoo seems to carry little (if any) risks of side effects – mainly because of its low time of exposure and systemic absorption versus its oral formulations.

The best candidates for 2% ketoconazole shampoo are hair loss sufferers who are comfortable using the shampoo 2-3 times per week and who are dealing with dandruff and/or excessive hair shedding from AGA or TE.

More information on the science behind ketoconazole – its mechanisms of action, supporting evidence, expectations for hair regrowth, and contraindications – can be found below.

What Is Ketoconazole?

Ketoconazole is more commonly mentioned by the brand name Nizoral®, and most people know about it as a shampoo.

Simply put, ketoconazole is an anti-fungal medication. It’s a drug commonly used to help improve fungal-related conditions – like dandruff, fungal infections, certain hormone-linked diseases, and even hair loss from fungal and non-fungal causes.

If it’s a fungal medication, why is it used for hair loss?

Because ketoconazole’s mechanisms of action – as an anti-fungal, anti-inflammatory, anti-androgenic, and pro-anagen agent – all overlap with the causes of telogen effluvium and androgenic alopecia.

Here’s how.

Ketoconazole’s anti-fungal properties help fight off yeast, fungi, and bacterial infections that can cause excessive hair shedding.

As an anti-fungal medication, ketoconazole may also have anti-inflammatory effects, especially in hair follicle sites.^[2]https://www.ncbi.nlm.nih.gov/pubmed/9669136

Many yeast, fungi, and bacteria feed off our dead skin as well as the oils our skin produces (i.e., sebum) which helps to lubricate our hair. Resultantly, these species can often be found residing in parts of our hair follicle – specifically, the infundibulum (i.e., the upper third of each hair shaft) and sebaceous glands.

However, sometimes too many yeast, fungi, and/or bacteria may colonize our sebaceous glands – leading to over-colonization. This is particularly true with the fungus-like yeast species Malassezia spp., which is found in 65% of healthy scalps.^[3]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367942/

Many of these species produce toxic byproducts (i.e. porphyrins) as part of their digestion of sebum. In cases of over-colonization, the accumulation of toxins elicits an inflammatory response in the sebaceous gland. Ironically, the body often responds by sending more sebum to the sebaceous glands – which would help to otherwise resolve the inflammation, but not in these instances. Rather, the excess sebum simply feeds these pathogenic microorganisms, and the process continues.

This is known as a sebum-feedback loop. At moderate levels, it leads to excessive dandruff. At higher levels, it triggers excessive hair shedding – often characterized as microorganism-driven telogen effluvium (TE).

Enter ketoconazole – a potent anti-fungal medication that can help kill off these pathogens and, in doing so, stop this feedback loop.

Ketoconazole damages the cell membranes of fungi and yeast.^[4]https://pubchem.ncbi.nlm.nih.gov/compound/Ketoconazole Specifically, it stops a fungus from producing ergosterol – a crucial part of the cell membrane that helps keep cellular content from leaking out as well as unwelcome substances from invading.

The end result?

Ketoconazole helps kill off pathogenic yeast/fungi, which then reduces scalp inflammation and helps resolve any excessive hair shedding (TE).

This is also why ketoconazole is such an effective treatment for scalp conditions caused by fungi – like dandruff and seborrheic dermatitis. Those conditions are also often caused by Malassezia spp. – the fungus-like yeast that is (fortunately) hypersensitive to ketoconazole.

Ketoconazole might help reduce inflammation in 30-50% of men with androgenic alopecia

Research shows that 30-50% of hair loss sufferers with androgenic alopecia (AGA) also have P. acnes and/or Malassezia spp. infections in the scalp. Just like with TE, the presence of these microbes may exacerbate inflammation, induce early hair shedding, and thereby accelerate the progression of AGA.

In these cases, anti-fungal and/or antibacterial shampoos tend to be useful – because they help to reduce the infections that are accelerating hair shedding in AGA.

Ketoconazole might have anti-androgenic effects in scalp tissues

Ketoconazole isn’t just an anti-fungal; it also has anti-androgenic properties when taken orally. And, while researchers have debated whether these findings extend to topically applied ketoconazole, at least one peer-reviewed paper makes a strong argument in its favor.

Specifically, this hypothetical model argues that topically applied ketoconazole has anti-androgenic properties.^[5]https://www.ncbi.nlm.nih.gov/pubmed/14729013 In particular, it may help reduce dihydrotestosterone (DHT) – the main hormone implicated in AGA – and in two ways:

• Inhibits 5-alpha reductase. This is an enzyme that converts free testosterone into DHT.
• Blocks androgen receptors. Androgen receptors are where DHT attaches to a cell to influence tissue function (i.e., hair follicle miniaturization). If androgen receptors are blocked, DHT cannot bind to these cells, and thus does not affect that tissue’s functionality.

Together, if ketoconazole has enough of a DHT-reducing effect in balding scalp tissues, it should help to improve AGA – similar to the ways in which treatments like finasteride work.

Ketoconazole may prolong the anagen phase of the hair growth cycle

At any given moment, roughly 85% of scalp hairs are in their growth (anagen) phase, while remaining hairs are either in a resting (catagen) or shedding (telogen) phase.

One defining characteristic of telogen effluvium (TE) is a large increase in the number of shedding versus growth phase hairs (i.e., increased telogen:anagen ratio). In TE, it’s not uncommon to see telogen:anagen ratios of 40-50% and beyond.

This is also observed in androgenic alopecia (AGA) – though to a lesser degree, as AGA is characterized more so by hair follicle miniaturization, less so by hair shedding.

Interestingly, one research team demonstrated that, for reasons unknown, ketoconazole appears to prolong the anagen (growth) phase of hair follicles affected by TE and/or AGA.^[6]https://www.ncbi.nlm.nih.gov/pubmed/18498517

This effect should help delay the progression of both conditions, and maybe even partially reverse them.

Summary of Mechanisms

Ketoconazole might improve telogen effluvium by:

1. Killing off pathogens in the scalp, thus normalizing excessive hair shedding triggered by microorganism-mediated inflammation
2. Prolonging the anagen phase of the hair cycle

Ketoconazole might improve androgenic alopecia by:

1. Killing off pathogens in the scalp, thus normalizing excessive hair shedding triggered by microorganism-mediated inflammation
2. Reducing scalp DHT levels by inhibiting 5-alpha reductase and blocking androgen receptors
3. Prolonging the anagen phase of the hair cycle

Altogether, these mechanisms suggest that ketoconazole may improve both TE and AGA. So, what’s the evidence in human studies?

Clinical studies: is ketoconazole effective for hair loss?

As is always the case with hair loss research, context is key. And when looking into the effectiveness of ketoconazole, we need to evaluate all clinical studies with several things in mind:

1. Was the ketoconazole tested on androgenic alopecia or other hair loss disorders?
2. Was the formulation strength 1% or 2%?
3. What, exactly, was measured?

To date, there are only four clinical studies on ketoconazole and hair loss (that we could find). As such, we’ll present them in detail. If you’d like, you can skip to the summaries of each study.

Ketoconazole Shampoo: Effect of Long-Term Use in Androgenic Alopecia

Full text: Piérard-Franchimont et al., 1998 ^[7]https://www.ncbi.nlm.nih.gov/pubmed/9669136

Study one: 2% ketoconazole versus a normal shampoo

• Who: 39 male only-AGA-subjects
• What: 2% ketoconazole shampoo versus a normal shampoo. During the study duration, 27 men used ketoconazole while 12 men used normal shampoo. There were also 22 non-AGA-controls – half of them testing ketoconazole; half of them trying normal shampoo.
• How long: 2-4 times per week for 21 months
• Measurement: AGA pilary index (PI). This was defined as the percentage of hairs in anagen (A) x average diameter (D, μm) of the hair shafts 1.5 cm from the hair bulb.
• Results:
  • PI of non-AGA-controls remained unchanged, no matter the type of shampoo used (ketoconazole versus normal shampoo).
  • PI of only-AGA-subjects with unmedicated shampoo showed a slow linear decrease over time, while the ketoconazole group “yielded a progressive PI increase that became evident after a 6-month survey and apparently reached a plateau value after about 15 months”.
• Takeaways:
  • In men without androgenic alopecia, ketoconazole doesn’t improve anagen hair counts or hair shaft diameter
  • In men with androgenic alopecia, ketoconazole improves both anagen hair counts and overall hair shaft diameter

Study two: 2% ketoconazole versus 2% minoxidil

• Who: 8 male only-AGA-subjects; 4 using ketoconazole, and 4 using minoxidil
• What: 2% ketoconazole shampoo (vs. 2% minoxidil lotion)
• How long: ad libitum (i.e., as often as desired) for 6 months
• Measurements: hair density; hair shaft diameter and the corresponding sebaceous gland
• Results:
  • “A 7% increase in the median hair shaft diameter was yielded by both the [ketoconazole] shampoo and minoxidil + unmedicated shampoo combination.”
  • “A 19.4% decrease in the mean sebaceous gland area was observed in the [ketoconazole] group. In contrast, the same variable increased by 5.3% in the minoxidil + unmedicated shampoo group.”
  • Ketoconazole improved density of hair by 18% compared to minoxidil by 11%.
• Takeaways:
  • Ketoconazole increases hair shaft diameter by 7%, similar to minoxidil
  • Ketoconazole decreases sebaceous gland size by nearly 20% – possibly due to its anti-fungal effects. In other words, ketoconazole kills off pathogens that over-colonize, and thereby over-enlarge, the sebaceous glands. This was unique to ketoconazole (minoxidil did not have this effect).
  • Ketoconazole improves hair density nearly twice as well as minoxidil

Key points:

These studies are all on men with AGA only, all of whom tested 2% ketoconazole as a shampoo.

The results all show significant improvements to hair density, as well as prolonged anagen phases and hair diameter. Moreover, one study also found that ketoconazole decreased sebaceous gland size – most likely a result of its ability to kill off pathogens overcrowding those sebaceous glands. For these reasons, it’s not unreasonable to assume that ketoconazole might also decrease sebum output.

Nudging hair shedding by antidandruff shampoos. A comparison of 1% ketoconazole, 1% piroctone olamine, and 1% zinc pyrithione formulations

Full text: Piérard-Franchimont et al., 2002 ^[8]https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1467-2494.2002.00145.x

• Who: 150 men presenting with telogen effluvium related to androgenic alopecia associated with dandruff, separated into three groups with different shampoos: 50 men on 1% ketoconazole, 50 on 1% piroctone olamine, and 50 on 1% zinc pyrithione
• What: 1% ketoconazole shampoo versus two other anti-dandruff shampoos
• How long: 2-3 times a week, for 6 months
• Measurements: hair shedding, hair density, anagen hair percentage, mean proximal hair shaft diameter, sebum excretion rates
• Results:
  • Pruritus and dandruff cleared rapidly in all three shampoo groups
  • Hair density remained unchanged in all three shampoo groups
  • Hair shedding decreased by 17.3% in the ketoconazole group, 16.5% in the piroctone olamine group, and 10.1% in the zinc pyrithione group
  • Anagen hair ratio increased by 4.9% in the ketoconazole group, 7.9% in the piroctone olamine group, and 6.8% in the zinc pyrithione group
  • Sebum excretion rate decreased by 4.8% in the ketoconazole group, 2.9% in the piroctone olamine group, and 5.5% in the zinc pyrithione group

Key points:

The men featured in this study have telogen effluvium and androgenic alopecia. And, encouragingly, it seems like 1% ketoconazole shampoo 2-3 times per week lessened hair shedding by ~20%, increased hair shaft thickness by ~5%, and decreased sebum output by ~5%.

The bottom-line: comparing across studies, 1% ketoconazole isn’t as impressive as 2%, but the results are still there. For men (and women) suffering from both TE and AGA, 1% or 2% ketoconazole might be a great intervention (among other treatments).

Comparative Efficacy of Various Treatment Regimens for Androgenetic Alopecia in Men

Full text: Khandpur et al., 2002 ^[9]https://www.ncbi.nlm.nih.gov/pubmed/12227482

• Who: 100 male only-AGA-subjects randomized into four groups:
  • 30 finasteride
  • 36 finasteride + minoxidil
  • 24 minoxidil
  • 10 finasteride + ketoconazole
• What: 2% ketoconazole shampoo + finasteride 1mg oral/day (vs. finasteride vs. finasteride + 2% minoxidil vs. 2% minoxidil)
• How long: 3 times a week for 1 year
• Measurements: patients’ self-assessment and physicians’ assessment. Photographs were taken.
• Results: finasteride + minoxidil and finasteride + ketoconazole reap the best improvement scores for both self- and physician-assessments. However, finasteride + minoxidil slightly outperformed finasteride + ketoconazole.

Key points:
2% ketoconazole works well as a combination therapy with finasteride.

Pilot Study of 15 Patients Receiving a New Treatment Regimen for Androgenic Alopecia: The Effects of Atopy on AGA

Full text: A.W. Rafi et al., 2011 ^[10]https://www.ncbi.nlm.nih.gov/pubmed/22363845

• Who: 15 AGA subjects with either atopic dermatitis or seborrheic dermatitis
• What: 2% ketoconazole shampoo. 8 subjects used NuH Hair + finasteride + minoxidil + ketoconazole, 5 using only NuH Hair, 1 using NuH Hair + finasteride + ketoconazole, 1 using NuH Hair + ketoconazole (a subject with seborrheic dermatitis)
• How long: ketoconazole usage 2-3 times a week for 9 months
  Measurements: Average time for hair regrowth, photo and investigator assessments
• Results:
  • Average time for hair regrowth
    • 30 days with NuH Hair + finasteride + minoxidil + ketoconazole
    • 30 days with NuH Hair + finasteride + ketoconazole
    • 60 days with NuH Hair + ketoconazole
    • 90 days with NuH Hair alone

Key points:
Ketoconazole works well as a combination therapy with finasteride and minoxidil, and it can also improve AGA even in men with atopic and/or seborrheic dermatitis.

Key points summary of clinical trials

• By itself and as a combination therapy, 2% ketoconazole improves AGA and TE by:
  • Increasing anagen (growth) hairs
  • Increasing hair shaft diameter
  • Increasing hair density
• Hair improvements from 2% ketoconazole seem to sustain, not wane (at least over 21 months of use)
• 2% ketoconazole increases hair density; 1% ketoconazole doesn’t

Very broadly speaking, ketoconazole alone might be a little bit less effective than minoxidil alone, but it also seems to be a better bet in some respects: more people respond to Nizoral for hair loss, its effects don’t wane over 21 months, and it targets AGA from multiple angles.

Applying Ketoconazole

If you want to get the most out of ketoconazole, here are some tips to maximize your chances of hair regrowth and use ketoconazole in the most effective way:

Opt for 2% prescription, not 1% over-the-counter

There is evidence that prescription-strength 2% ketoconazole is (much) more effective than 1 % ketoconazole.

In this study, 2% ketoconazole shampoo increased hair density by 18% while in this study, 1% ketoconazole shampoo didn’t change hair density at all. Both times, ketoconazole was applied around 3 times a week for 6 months. ^[11]https://www.ncbi.nlm.nih.gov/pubmed/9669136 ^[12]https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1467-2494.2002.00145.x

Also, in this study, 1% ketoconazole and 2% ketoconazole were compared with their effect on seborrheic dermatitis, and the results were so that “[ketoconazole] 2% had superior efficacy compared to [ketozonaole] 1% in the treatment of severe dandruff and scalp seborrheic dermatitis.”^[13]https://www.karger.com/Article/PDF/51628

So get the 2% ketoconazole, not the 1%.

How can I get the 2% Nizoral shampoo without a prescription?

One of our members found 2% ketoconazole online, and from a company called Nizoral Shop.

So how does this company was circumventing prescriptions and shipping to the U.S. (and elsewhere)?

As it turns out, their Nizoral products depart from overseas warehouses where prescriptions are not required.

So, for anyone looking for 2%, Nizoral Shop might be a great option. The company later offered our members a 20% discount on the first 100 orders from our community.

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To access case studies, expert interviews, forums, comprehensive guides, and other special offers, join our membership. You will also get a personalized Regrowth Roadmap tailored to your needs and treatment preferences.

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We aren’t affiliated with any physical product brands, and we haven’t tried this shampoo brand. The company did say that for anyone making orders during the COVID-19 period: “It is highly recommended to select UPS/DHL priority express shipping option, as the other shipping methods are suspended until further notice due to the current pandemic.”

Get the Nizoral shampoo, not the topical

This is just a practical tip. In some countries, there is a topical version of ketoconazole available to consumers. Arguably, as a topical, ketoconazole would likely have more significant effects versus a shampoo – mainly because of the differences in the length of time on the scalp.

At the same time, topical ketoconazole may be more likely to cause side effects due to higher systemic absorption. What’s more, the topical non-shampoo version of ketoconazole has never been used in human studies on hair loss.

So, we recommend sticking to what’s studied; not what’s theoretically potentially more effective. Go with Nizoral shampoo.

Apply 2-4 times per week

Collectively, these studies show that applying 2% ketoconazole 2-3 times per week seems to show the most promise at resolving hair loss disorders and not just dandruff. So, plan on using this shampoo around every other day.

Do I have to use it forever?

Not necessarily. If ketoconazole’s most beneficial mechanism of action is that it kills off the over-colonization of pathogenic organisms that are creating additional scalp inflammation, then chances are that after these pathogenic organisms are gone, you may be able to significantly reduce usage frequencies after months 3-4.

That means transitioning to once-weekly usage (or less).

Combine ketoconazole with other hair loss therapies and treatments

Generally speaking, in ketoconazole studies on humans with AGA, the best results have been achieved by those that used ketoconazole in combination with other treatments.

This makes sense, as ketoconazole’s mechanisms of action are different from minoxidil, which are different from microneedling, which are different from finasteride. The more mechanisms you target, the better your results (in most cases).

In fact, we have an example from our community of a member doing just this: combining ketoconazole with microneedling, massaging, and minoxidil to break through a period of stagnation in hair recovery.

Here are his results: 20+ months of scalp massage alongside microneedling, minoxidil, and ketoconazole

Nizoral for Hair Loss: The Side Effects

This study showed that high doses of oral ketoconazole can impair testosterone production in men, but this review article from drugs.com states that these effects haven’t been reported – even with topical ketoconazole – and seem unlikely anyway because through topical application, way too little substance is absorbed.^[14]https://www.ncbi.nlm.nih.gov/pubmed/3659003^[15]https://www.drugs.com/monograph/ketoconazole-topical.html

So, based on this information, you don’t need to worry about the shampoo’s effect on testosterone.

Rare side effects are summarized here. These are not prevalent, particularly if ketoconazole is formulated as a shampoo.^[16]https://www.drugs.com/sfx/ketoconazole-topical-side-effects.html

All in all, ketoconazole shampoo seems to be relatively free of side effects, and a relatively safe option for those with excessive hair shedding from androgenic alopecia, telogen effluvium, or both.

For those with sensitive skin who wish to try a more natural Nizoral formulation, Sent from Earth Caffeine & Saw Palmetto Shampoo may suffice. However, this shampoo contains just 1% ketoconazole. We are not affiliated with this company; we just wanted to provide an example of what else is out there.

Who are the best candidates for Nizoral?

In regard to hair loss sufferers, ketoconazole is proven to help:

Those with androgenic alopecia

Having checked the studies above, it is pretty indisputable that ketoconazole improves AGA in humans – and not only in those who suffer additionally from seborrheic dermatitis or telogen effluvium, but clearly also in those who have only AGA. ^[17]https://www.ncbi.nlm.nih.gov/pubmed/9669136

Those with a hair shedding disorder (like telogen effluvium)

When TE is derived from a pathogenic microorganism, seborrheic dermatitis, or both (which can be the case), ketoconazole might help – as its anti-fungal effects can intervene in the earliest stages of seborrheic dermatitis development.^[18]https://donovanmedical.com/hair-blog/2017/5/23/is-it-possible-for-seb-derm-to-cause-hair-loss

Interestingly, ketoconazole seems to improve TE regardless of its causes. We know this from the above study with 150 TE men, which showed that ketoconazole improved TE outcomes – despite the high likelihood of myriad TE causes present within that study.^[19]https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1467-2494.2002.00145.x

These studies are mostly on men. What about women?

To our knowledge, there are no published studies on Nizoral for hair loss in females with pattern alopecia (yet). However, one study on females found that 2% ketoconazole as a topical (not shampoo) demonstrated similar efficacy compared to 2% minoxidil over six months of use.^[20]https://biomeddermatol.biomedcentral.com/articles/10.1186/s41702-019-0046-y

Given the results of this study (and ketoconazole’s suspected mechanisms of action), there is reason to believe ketoconazole shampoo is probably effective for women, as well.^[21]https://www.derm.theclinics.com/article/S0733-8635(12)00093-9/abstract

You’re an ideal candidate for ketoconazole if you…

• Suffer from AGA and/or a hair shedding disorder, particularly alongside seborrheic dermatitis or symptoms of microorganism overgrowths (like excessive dandruff and/or sebum activity)
• Want the benefit of a chemical treatment without a high risk of severe side effects
• Are using minoxidil/finasteride and want to increase their efficacy
• Are performing stimulation-based therapies (i.e., massaging, microneedling, and/or platelet-rich plasma) and want to speed up the regrowth process.

Who is not a good candidate for ketoconazole?

Ketoconazole is less researched on women, although that doesn’t make it less effective. But there are contraindications for oral ketoconazole in pregnant women – and, as a precaution, the standard recommendation is for all women who intend on getting pregnant to avoid even the topical formulations.^[22]https://www.drugs.com/pregnancy/ketoconazole.html

Regarding mothers who breastfeed, ketoconazole use is generally considered acceptable, but caution is recommended.^[23]https://www.drugs.com/breastfeeding/ketoconazole.html

Above all, both men and women are strongly advised against the use of oral ketoconazole for the treatment of AGA/pattern hair loss. While topical/shampoo formulations have a strong safety profile, oral ketoconazole doesn’t. Consequently, it comes with a higher risk of side effects and is even banned from sale in certain countries.

Summary

Ketoconazole isn’t as well-researched as minoxidil or finasteride. However, studies show that it might be an effective add-on treatment for hair loss (specifically, androgenic alopecia).

There’s evidence that ketoconazole is almost as effective as minoxidil (Rogaine®) at increasing hair density… and that it might be particularly helpful for those with pattern hair loss with rapid hair shedding (i.e., telogen effluvium). So, if you fit within these categories, you might want to consider trying it.

Having said that, ketoconazole formulation matters. While 1% over-the-counter ketoconazole might help reduce dandruff and improve hair loss, 2% prescription ketoconazole is likely superior in its ability to improve hair loss outcomes. So, if you’re going to commit to Nizoral for hair loss, commit fully. Visit your doctor and get a prescription. Or, order online from the Nizoral Shop. Then, start shampooing.

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

In this article, we’ll review 

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

Interested in Topical Finasteride?

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

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

Click Here For 15% Off

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

About Finasteride 

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

Oral Finasteride

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

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

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

Topical Finasteride

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

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

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

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

Serum vs Scalp DHT 

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

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

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

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

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

Topical Finasteride Can Still Go Systemic

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

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

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

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

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

So Just Reach for the Lowest Percentage, Yes?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

So What’s the Perfect Amount and Formula?

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

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

Join our Membership Program to get the full analysis.

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

How to Maximize Gains and Minimize Side Effects

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

1. Get Lab Tests for DHT

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

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

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

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

2. Understand That DHT Levels Fluctuate Diurnally

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

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

3. Avoid supplementing with Quercetin and/or Creatine

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

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

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

4. Set Realistic Expectations and Track Progress

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

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

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

Summary

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

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

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

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

Studies show that within 3-6 months of stopping minoxidil, any hair growth resulting from the drug is lost. After quitting minoxidil, hair counts can even temporarily fall below where they would’ve been had we never sought treatment at all, before eventually rebounding back to baseline.

Why does this happen? Is there a way to lessen the “withdrawal shed” from minoxidil? For those who’ve seen hair gains with minoxidil but prefer not to use it forever, there may be some methods to mitigate shedding after quitting minoxidil. This article explains the evidence, and provides an action plan.

• About Minoxidil
• Why People Stop Taking Minoxidil
• What Happens When Quitting Minoxidil
• Is Minoxidil Plus Microneedling the Answer?
• How to (Possibly) Prevent Shedding After Stopping Minoxidil

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About Minoxidil

Minoxidil is an over-the-counter drug approved by the FDA to treat androgenic alopecia. It’s commonly known by the brand name Rogaine. Along with finasteride, minoxidil is one of only two drugs approved to treat androgenic alopecia in both men and women.

Nobody actually knows how minoxidil works. Minoxidil was initially developed in the 1980s as an oral drug to treat high blood pressure. But when patients started reporting “unwanted” hair regrowth after three or more months of use, its manufacturers decided to reformulate it into a topical and begin testing it on men with androgenic alopecia.^[1]https://www.jaad.org/article/S0190-9622(08)00809-8/abstract

Today, we still aren’t sure how it works. But since side effects are minimal, it was nonetheless approved by the FDA for use. There are two primary hypotheses on the mechanisms behind minoxidil. 

Hypothesis 1: Minoxidil is a Vasodilator

One defining characteristic of androgenic alopecia is reduced blood flow to balding regions. While there’s debate over whether reduced blood flow is a consequence or cause of hair loss, it’s undisputed that without proper blood supply to a hair follicle, hair cannot grow. 

As a vasodilator, minoxidil widens blood vessels, potentially increasing blood flow to the scalp. In addition, Minoxidil opens potassium ion channels, which some researchers think works alongside vasodilation to improve hair growth.^[2]https://pubmed.ncbi.nlm.nih.gov/9395721/ 

Hypothesis 2: Minoxidil Alters the Hair Growth Cycle

It’s possible that minoxidil kicks miniaturizing hair follicles back into the anagen (growth) phase of the hair cycle. Hairs thus become thicker, giving the appearance of overall improved hair density. This could be the result of minoxidil decreasing prostaglandin D2 levels while boosting other prostaglandins, like prostaglandin E2, to downregulate pro-inflammatory growth factors that are linked to hair shedding.^[3]https://www.jidonline.org/article/S0022-202X(15)42806-4/pdf 

In addition, Minoxidil may prolong the growth phase of the hair cycle by maintaining beta-catenin activity in dermal papilla cells.^[4]https://pubmed.ncbi.nlm.nih.gov/21524889/ 

How Long Does Minoxidil Take to Work?

Minoxidil’s event horizon is approximately 3-6 months. Over half of the people who try it respond to minoxidil within this time frame. But early results tend to wane over time.

One study found that at six months, men using 5% minoxidil twice-daily saw a near-60% change in hair ‘weight’ in balding regions.^[5]https://www.sciencedirect.com/science/article/pii/S019096229970006X In other words, their hair had thickened or regrown to weigh 60% more than it did at the start of the study. 

That’s huge. 

Unfortunately, the same study showed that at 96 weeks, those hair weights decreased to merely 25% higher than baseline. This also happens to be a consistent finding across most studies on minoxidil. Just see this 48-week chart on the effects of 2% and 5% minoxidil on hair counts.^[6]https://pubmed.ncbi.nlm.nih.gov/12196747/ Results tend to peak at week 16, then decline thereafter.

This is echoed on 5-year studies on minoxidil, which show a steady decline in non-vellus hair counts in target areas after year one: ^[7]https://pubmed.ncbi.nlm.nih.gov/2180995/

Somewhat relatedly, other studies have demonstrated greatly increased hair counts that failed to translate to visual improvements in hair density.^[8]https://www.jaad.org/article/S0190-9622(08)00809-8/abstract

Long-story short: over time, minoxidil’s efficacy begins to wane. And while minoxidil can temporarily increase hair counts, these increases don’t always lead to cosmetic levels of hair regrowth.

Why is this? 

Minoxidil helps kickstart hairs back into the anagen (growth) phase of the hair cycle. However, it doesn’t address DHT-driven hair follicle miniaturization. So, while hair counts increase, hair diameters continue to decline, leading to a loss of hair volume and thereby hair thinning over time. 

Most people who try minoxidil quit within a year as their results stabilize or slowly decline.  

Let’s take a closer look at why, and what happens when they do.

Why Stop Taking Minoxidil?

People who stop taking minoxidil tend to fall into two main camps. Either minoxidil is just not working for them at all, or it is working, but for various reasons, they’d prefer to pass on a twice-daily application for the rest of their lives.

Minoxidil Non-Responders

Some people simply don’t respond to minoxidil. This could be a sign their hair loss stems from a condition other than androgenic alopecia. But as we’ll see, minoxidil just doesn’t always work well on its own. 

Is it Androgenic Alopecia?

Non-response to minoxidil could signify that hair loss is not due to androgenic alopecia but something else. There’s some evidence that oral minoxidil might improve hair shedding disorders like chronic telogen effluvium, but it’s technically not FDA-approved for that condition.^[9]https://link.springer.com/article/10.1007%2Fs40257-018-0409-y

Is it Strong Enough?

When choosing between 2% and 5%, choose the more potent formula. Studies show that in men, 5% minoxidil is better than the 2% formula, and the same is likely true for women. Prescriptions are available for concentrations of 10% or 15%, and studies show minoxidil non-responders often see better hair growth after switching to these strengths.^[10]https://pubmed.ncbi.nlm.nih.gov/28078868/

Is it in Use as a Monotherapy?

The reality is that minoxidil just isn’t very effective by itself. To understand why it helps to learn about an enzyme called Sulfotransferase.

In order to become active, minoxidil must come into contact with Sulfotransferase. About 40% of balding men just don’t have enough Sulfotransferase to elicit a response to Minoxidil – which happens to closely correspond with the percent of non-responders of minoxidil.

What might help increase Sulfotransferase levels? We’ll get to that later.

The Downsides of Minoxidil

Even minoxidil responders may not want to use it forever. It can be costly and inconvenient, and it does have some minor side effects.

Cost

Monthly minoxidil use costs between $15-$40. Hair loss sufferers will need to try it for 6 months and spend close to $200 just to see if they’re a responder. Stick with it for years, and they could end up spending thousands. Some users find that as their results taper off, it no longer warrants the ongoing expense.

Note: the price of minoxidil can be dramatically reduced by purchasing in bulk and through big brands – like the minoxidil offered from Kirkland. But these formulations tend to come with propylene glycol and other carrier ingredients that can irritate the scalp.

Side Effects

The biggest side effect of minoxidil seems to be skin irritation. Between 2% to 6% of users report this.^[11]https://www.researchgate.net/publication/221695328_Minoxidil_Use_in_Dermatology_Side_Effects_and_Recent_Patents However, allergy testing suggests that up to 80% of skin-irritation related side effects from minoxidil may not be caused by the minoxidil itself, but rather, a carrier ingredient called propylene glycol.^[12]http://www.thaiscience.info/Journals/Article/JMAT/10986429.pdf

There are brands that offer minoxidil without propylene glycol, so be sure to check the labels if you have any concerns of allergies.

Additional side effects include toxicity to cats, under-eye bags, and potential heart palpitations. But these are all relatively rare.

Inconvenience

As hair growth treatments go, minoxidil is relatively easy and convenient. Still, not everyone wants to commit to twice-daily use for the rest of their lives, regardless of its effectiveness. And as we mentioned earlier, minoxidil alone is not an effective long-term treatment. To keep results from waning, using minoxidil in combination with other therapies is recommended, which only adds time and expense.

So if someone decides to stop taking minoxidil, what are the expectations? 

What Happens When Stopping Minoxidil

In 1999, researchers conducted a study on the effects of abruptly ceasing minoxidil after long-term treatment.^[13]https://www.jaad.org/article/S0190-9622(99)70006-X/fulltext Not only did the group who stopped minoxidil shed hair, but for a month or two, they actually crossed below the threshold of where they would have been if they’d never used minoxidil to begin with. 

Let’s take a closer look at what happened.

The Study on Stopping Minoxidil

Researchers spent more than two years following four separate cohorts. One group was treated with 2% minoxidil, another group with 5%, one group was given a placebo, and the fourth group did nothing.

Both the 2% and 5% groups saw improvements in hair counts by the three-month mark. As we’ve said, these improvements leveled off a bit from that point forward but were still higher than hair counts in the placebo and control groups. 

After almost two years of treatment, at the 96-week mark, the investigators took the people in the 2% and 5% minoxidil groups and discontinued treatment. We can see the exact moment this occurred by looking at the data on hair weights, which soon started decreasing.

Three months later, by week 108, their hair loss had dipped well below the placebo group and below where they were at the start of the study. Another three months after that, by week 120, both the 2% and 5% groups had rebounded to rejoin toss sufferers will end up right where they started. 

As mentioned, any excess shedding should not be permanent, as hair will readjust to new homeostasis without the drug. 

So the question becomes, is there a method to weaning from minoxidil that can prevent or reduce shedding?

Is Minoxidil Plus Microneedling the Answer?

In the above study, minoxidil was used as a monotherapy. And we know from the research that combining minoxidil with additional therapies, such as microneedling, can improve outcomes for non-responders and may prevent results from waning after the initial 3-6 months of usage.

So could microneedling also prevent (or delay) shedding if one decides to stop taking minoxidil? Let’s investigate what happens when we use these two therapies in tandem. 

About Microneedling

Microneedling is a micro-wounding procedure that involves pricking the skin with tiny needles using either a roller or a pen-shaped tool.  Studies have shown microneedling elicits growth factors, signaling proteins, and the enzymatic activity of Sulfotransferase, which we referred to earlier.

In some studies, Microneedling plus Minoxidil seems to elicit a fourfold greater effect on hair count increases than Minoxidil alone.^[14]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746236/

In fact, when combining minoxidil with microneedling, new data show that all new hair gains might hold for much longer – even after quitting all treatments.

The Data on Combined Therapies

Let’s take a closer look at a 2020 study to see why microneedling could be the key to maintaining hair growth, even after quitting minoxidil.^[15]https://pubmed.ncbi.nlm.nih.gov/29028377/

In the study, researchers split men into 3 groups. One treated their hair loss with minoxidil only, another group with microneedling only, and one group combined the two therapies. As other studies have shown, the combined therapies were significantly more effective in terms of hair growth.

But what the researchers did next was interesting. They stopped all treatments for each of the 3 groups, then brought them in 6 months later to ask, ‘how much hair growth did you retain, even in the absence of treatment?’ Here were their results:

• Minoxidil Only – 90% lost all new hair growth (just 10% retained new growth)
• Microneedling Only – 70% retained some new hair, 20% retained all new hair, 10% lost all new hair
• Combined Therapies – 70% retained some new hair, 20% retained all new hair, 10% lost all new hair

So the group that combined minoxidil with microneedling not only experienced at least twice the hair growth of the other two groups, but 70% of them held on to at least some of this new growth, even after stopping all treatments. And yet, before we conclude that microneedling plus minoxidil is a fail-safe method for maintaining hair growth after treatment ends, there are some possibilities to consider.

1. It’s possible if researchers asked the same question 12 months versus 6 months later, all groups would report an equal amount of hair loss. We’ve seen with other therapies, Finasteride for example, that gains disappear over a longer timeline.
2. While the number 70% sounds big, the sample size in this study was relatively small. Each group contained just 20 men. So, while it’s great that 14 men maintained at least some of their results for 6 months after treatment ended, it’s possible this percentage could change within a larger sample.

So, while the study above is promising, we don’t really have enough data to definitively say whether or not hair shedding after quitting minoxidil can be prevented. 

We’ve yet to see any literature that would help predict who will or will not shed badly from minoxidil. However logically, it may be that those who respond better to minoxidil (or the more hair minoxidil helps one keep during use) simply have more hair to lose during withdrawal.

Anecdotally, about 50% of the male Perfect Hair Health members who have slowly weaned from minoxidil while maintaining microneedling therapy noticed no cosmetic differences in their hair counts afterward. 

Basically, they’re able to maintain similar visuals even without the drugs. The other 50% do see a decline visually, but it’s nowhere near baseline or very rarely all the way back to baseline.

If hair loss sufferers do get to a point where they’re happy with their hair and want to wean away from drugs, doing so with the right tapering protocol while continuing the use of microneedling could be a solution. 

The Best Way to Quit Minoxidil

When is the best time to call it quits? Never, if you’d like to take as much risk off the table as you can.

Otherwise, the following tips may help minimize any shedding related to minoxidil withdrawals.

• Start microneedling before quitting. Minoxidil and microneedling are synergistic treatments. Try them together for at least 3-6 months before dropping the drug.
• Don’t quit cold turkey. Follow a tapering protocol to minimize abrupt changes to the scalp environment. (We have a detailed weaning protocol in our membership.)
• Continue with alternative treatments. An effective weaning protocol takes up to 6 months. Continue with microneedling during this time.
• Replace minoxidil with natural therapies. Individuals may wish to experiment with other topicals instead, such as 2-5% rosemary oil. 

For the most part, minoxidil requires lifelong use to hold onto any hair maintained or regrown. As such, shedding often occurs for 3-6 months following a stop in minoxidil application. But, we can significantly mitigate this shed by combining minoxidil with additional therapies and following a tapering protocol.

Summary

Minoxidil can be an effective treatment for androgenic alopecia, although research says when used alone, results taper off over time. Combining minoxidil with wounding therapies such as microneedling can make it more effective.

When stopping minoxidil, hair loss can be expected. Research shows losses will be greatest within the first 3-6 months of quitting but will eventually rebound to where hair counts would have been had minoxidil never been applied. 

This doesn’t mean hair loss sufferers are stuck taking minoxidil for the rest of their lives. The same microneedling therapies that make minoxidil more effective may help sustain results after quitting the drug. This is especially true for those who commit to a strict tapering protocol versus quitting minoxidil cold turkey.

So should people use minoxidil? 

For many, it’s worth a try. Some people will see visual improvements, some of which can be maintained with a proper weaning program. In the worst case, people will most likely end up where they would’ve been without treatment, but not worse off. 

Minoxidil is just one of two FDA-approved hair loss drugs. But FDA-approval doesn’t necessarily equate to guaranteed results with Minoxidil. In fact, many hair loss sufferers use minoxidil (i.e., Rogaine®) for six months and still don’t see significant benefits.

Why is that? In other words, why do 50% of people seem to respond favorably to minoxidil, while the remaining 50% see little-to-no benefit?

Research suggests this split in regrowth might be tied to an enzyme in the hair follicle called sulfotransferase.

Without coming into contact with sulfotransferase, Minoxidil won’t have an effect, and about 40% of men just don’t have enough sulfotransferase to elicit a response to Minoxidil. 

Minoxidil is a pro-drug, meaning it has to be activated before it can exert its effects. Sulfotransferase plays an irreplaceable role in this because it turns minoxidil (its pro-drug form) into minoxidil sulfate (its active form).

We call this a rate-limiting step in the response rate to topical minoxidil, meaning the individual activity of the sulfotransferase enzymes on your scalp will predict your response rate to minoxidil.

This enzyme is also found in the liver. When oral minoxidil is ingested, it passes through these sulfotransferase enzymes, where it’s then distributed to the hair follicles throughout the body.

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When Can Responders Expect to See Visible Regrowth from Minoxidil?

First, let’s talk about the event horizon for Minoxidil. With Minoxidil, results can be expected a little faster than Finasteride, so typically shedding is experienced between two and four months, but then re-growth is usually cosmetically perceptible around the one month to six-month mark. This makes sense, as Minoxidil acts more like a stimulant, or growth agonist. 

Minoxidil turns more hairs on; it doesn’t necessarily target miniaturization. So Minoxidil doesn’t have as dramatic of an impact on reversing hair miniaturization and thereby improving hair thickness, but it can help to create a denser, fuller head of hair.

For those looking to reverse hair thinning, here are three ways to enhance the effectiveness of minoxidil treatment.

1. Acute Wound Generation via Microneedling

One of the easiest ways to enhance the efficacy of minoxidil is through acute wound generation, which is best administered through microneedling and massage. 

Microneedling plus Minoxidil seems to elicit a four-fold greater effect of hair count increases than just Minoxidil alone.

Microneedling elicits growth factors, signaling proteins and enzymatic activity of sulfotransferase. Microneedling may also increase topical absorption and potentially even attenuate scarring – all of which pair well with minoxidil use.

Researchers started testing minoxidil + microneedling as a combination treatment back in 2013 – with incredible results.

One study showed over 12 weeks, minoxidil+ microneedling increased minoxidil efficacy four-fold and led to a 40% increase in hair count – with real, visual hair changes.^[1]http://www.ijtrichology.com/article.asp?issn=0974-7753;year=2013;volume=5;issue=1;spage=6;epage=11;aulast=Dhurat

More recently, this study showed that over 6 months, minoxidil + microneedling had a 100% response rate and led to a 25% increase in hair count.^[2]https://www.tandfonline.com/doi/abs/10.1080/14764172.2017.1376094?journalCode=ijcl20

It’s suspected that these improvements are due to microneedling’s ability to: 

1 – Enhance skin enzymes required to activate minoxidil (i.e., sulfotransferase), 

2 – Improve the absorbability of topicals like minoxidil – since the wounding allows for easier access to hair follicles and their blood supply, and 

3 – Potentially attenuate or partially reverse fibrosis.

As with microneedling, Perfect Hair Health’s standardized scalp massages may help responders increase hair counts.

2. Switch to higher concentrations 

Studies show that minoxidil non-responders see better hair growth after switching to 10% or 15% minoxidil. One such study was conducted on women with female pattern hair loss who were non-responders to 5% Minoxidil. They were trialed with 15% Minoxidil topically, and 70-80% of them saw a significant response. Participants saw an average of about 13% increase in hair counts.^[3]https://clinicaltrials.gov/ct2/show/NCT02486848

So moving from 5% as a non-responder to 15% can really improve results.

Anecdotally, 15% Minoxidil is relatively safe. There’s not a ton of data on it, but when looking at the half-lives of Minoxidil, its transfusion into the system, and how much circulates from topical application, it doesn’t seem like there’s a massive uptake in the systemic volume of Minoxidil from going from 5% to 15%, at least from a biological perspective.

3. Add in topical retinol / retinoic acid 

Another way to improve sulfotransferase activity? Using Tretinoin or Retinoic Acid. These are Vitamin A derivatives that help to activate sulfotransferase activity, stimulate a little bit of inflammation and cell turnover and in doing so, make minoxidil way more effective.

Topical minoxidil is delivered as a “pro-drug” – meaning that it is not technically active when it touches the scalp skin. Rather, minoxidil has to come into contact with an enzyme called sulfotransferase. 

Unfortunately, many men and women don’t have enough sulfotransferase activity in the skin to elicit a major hair change with minoxidil alone. Fortunately, adding in topical retinol / retinoic acid can increase the activation of sulfotransferase, and thereby minoxidil – potentiating even bigger hair gains. 

Just a few short years ago, hair loss sufferers had to ask their doctor to write a prescription for Vitamin A derivatives. There are brands online that sell combination formulas – like Happy Head, Adegen®, and MinoxidilMax. No doctor visit is required.

These companies sell products, but are these companies actually legitimate? Do their products actually contain the advertised ingredients? How do these formulas stand up to our rigorous lab tests? Join the Perfect Hair Health Membership Program to find out. 

Summary

About 60% of people seem to be hyper-responders to Minoxidil. They see great hair count increases, and usually, they’ll see this in the first six months of treatment. Then those hair count increases will steadily decline over time. For the other 40% of people who try Minoxidil, there’s zero effect.

For high-responders, there is utility in taking a more multifactorial approach to Minoxidil treatment, where microneedling, high-concentration Minoxidil, and retinoic acid are combined to accelerate hair growth.

Stool transplants – also known as fecal microbiota transplants (FMT) – are a controversial therapy reserved for life-threatening bacterial infections and autoimmune disorders. Fascinatingly, people who’ve undergone stool transplants have later reported unintended benefits: weight loss, less acne, personality improvements, and even hair regrowth.

At face value, a connection between stool transplants and hair loss sounds like science fiction. How could altering the bacteria inside of our guts affect hair growth on top of our scalps?

At the same time, new research suggests that the hair loss-fecal microbiota connection is very real, and may even become a future therapeutic target for people looking to regrow hair.

In this article, we’ll dive into the science surrounding stool transplants: what this therapy is, what it does to our gut microbiome, and the evidence linking fecal microbiota transplants to hair regrowth in alopecia areata, telogen effluvium, and maybe even androgenic alopecia.

We’ll even showcase a few before-after photos featured in studies and forums from people who received stool transplants to treat unrelated health conditions, and ended up (accidentally) experiencing hair regrowth.

If you have any questions, feel free to reach us in the comments below.

Table of contents

• What is a stool transplant?
• Alopecia areata
• Telogen effluvium
• Androgenic alopecia

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What is a fecal microbiota transplant (i.e., stool transplant)?

Our guts are like a storage facility for large colonies of microbes. Because of the role the gut microbiome encompasses, many diseases and conditions that relate to a dysfunctional gut microbiome, have now been treated utilizing a fecal microbiota transplant.

An artist’s rendering of gut organisms and debris

A fecal microbiota transplant (FMT) is basically what it sounds like: the transfer of stool from one individual’s colon into another person. The aim? To improve gut bacteria density and diversity. In other words: increase the total number of “good” bacteria in the gut, as well as the number of “good” species.

Stool transplants – or FMTs – are nothing new. This practice has been around since the 4th century. More recently, it gained notoriety when the FDA approved FMTs for recurrent Clostridium difficile infections – a deadly bacterial infection that often grows resistant to antibiotics [1].

In this context, FMT’s are incredibly successful. For a benchmark, antibiotic treatments for C. difficile tend to boast a 20-30% remission rate. FMTs boast around a 90% remission rate [2]. In the veterinary world, FMT’s are used for similar purposes [3].

While the use of a FMT seems most pertinent to gastrointestinal diseases, there is a much broader spectrum for the therapy in relation to other conditions, such as multiple sclerosis, Alzheimer’s disease, epilepsy, obesity, and metabolic syndrome (to name only a few) [4, 5].

Can fecal microbiota transplants alter our gut microbiome?

FMTs are perhaps one of the most powerful ways to alter our gut microbiome: the collection of bacteria inside our intestines that help regulate anything from autoimmune reactions to hormonal levels to nutrient metabolism.

C. difficile & stool transplants: alterations to gut flora

In one study, researchers decided to investigate 55 stool samples from donors and recipients who used FMTs as a treatment for C. difficile infections. They found major differences in the pre- versus post-procedure samples of the recipients [6].

Before the procedure, healthy donors’ stools contained a significant portion of the phylum of bacteria – known as Firmicutes and Bacteroides – constituting roughly 85% of bacteria identified.

We can first think of a phylum as the link between different species of bacteria. For example, while an oak tree differs from a palm tree, ultimately, they’re still all trees. As such, no one group can be labeled as good or bad as often the species within those groups can exhibit both helpful and disruptive properties. This is evident with helminth infections – where the same helminth can cause inflammation in the first-world but protect from malaria in the developed world.  To put it simply: the effects of a bacteria often rely on its environment, the health of an individual, the ratio of that bacteria to others, and about a billion other factors [7,8].

However, in the case of resistant Clostridium infections, Firmicutes and Bacteroides tend to be absent. This suggests that these phylum may play a role in preventing gut dysbiosis and thereby C. difficile overgrowths.

With respect to the study, here’s what researchers found:

• Prior to the stool transplants, recipients’ stools had lower amounts of Firmicutes and Bacteroides and markedly high Fusobacteria and Proteobacteria.
• Donor stool contained exceptionally higher Firmicutes and Bacteroides, as well as lower Fusobacteria and Proteobacteria.
• After treatments, recipients’ stool showed the higher Firmicutes and Bacteroides as well as lower Fusobacteria and Proteobacteria (thereby more closely resembling that of the donor’s gut).
•  After transplantation, the more closely a recipient’s gut matched that of its donor, the more likely that recipient was to experience a remission from C. difficile.

In other words, FMTs significantly altered gut flora – and to the benefit of sick patients.

Interestingly, the health of our gut microbiome is linked to many hair loss disorders – particularly alopecia areata and telogen effluvium. Moreover, research now links gut bacteria to the regulation of DHT – the hormone implicated in pattern hair loss.

We’ll dive into this evidence below: what it is, what it means, and why it might rewrite a lot of what we think we know about hair loss.

Stool transplants for hair loss: the evidence

When it comes to FMTs as a treatment for hair loss, evidence is very limited. This is because reports of fecal transplants and hair regrowth have mainly happened by accident – specifically, after a patient with C. difficile + hair loss receives a stool transplant and later inadvertently sees improvements to both conditions.

Nonetheless, there is compelling evidence of a gut microbiome-hair loss connection. To best outline this evidence, we’ll dive into the research on FMT’s and hair loss as organized by :

1. Alopecia Areata
2. Telogen Effluvium
3. Androgenic Alopecia

Let’s begin.

Alopecia areata and fecal microbiota transplants

Alopecia areata (AA) is an autoimmune form of hair loss; it often presents as patchy-related hair loss in the scalp. Researchers currently believe AA is the result of a collapse in “immune privilege” of the hair follicles – whereby the immune system begins to read hair follicles as foreign invaders, and then starts to attack them.

Alopecia areata: patchy hair loss

When it comes to stool transplants, alopecia areata is the best-studied form of hair loss. This isn’t saying much – because there’s not a ton of data on stool transplants and hair regrowth in general. Again, the studies here have been unintended and inadvertent: people with alopecia areata seem to have higher rates of gut dysbiosis, and thereby they seem to suffer disproportionately from infections like C. difficile. Therefore, they’re probably more likely to eventually become eligible for extreme treatments like a stool transplant – which is why we have case reports of FMTs and AA-related regrowth in the first place.

So, what limited evidence do we have on stool transplants for hair regrowth from alopecia areata?

Case reports of FMTs and hair regrowth from alopecia areata

Study #1: two uncontrolled retrospective case reports

In a study where two patients received an FMT for treating Clostridium difficile, researchers reported that both people saw an unintended benefit of hair regrowth following the procedure [14]. In these cases, both patients were classified as having alopecia universalis – an advanced form of alopecia areata where the hair loss has progresses beyond the scalp and to the body.

In the first case, the 38-year old man began to grow peach fuzz not only on his head, but also his face and arms. The regrowth became cosmetically noticeable 8 weeks after the stool transplant – after having suffered from progressive alopecia universalis for decades without any improvements.

In the second case, a 20-year old man – diagnosed with alopecia universalis 2 years prior to his FMT – saw major improvements to scalp hair regrowth over a 1.5-year period after receiving a stool transplant. Prior to the FMT, this subject had tried to treat his alopecia using corticosteroid injections, topical steroids, squaric acid, and laser treatments— all to no avail. While this man also received steroid injections within his scalp after the FMT, he began to grow hair throughout the rest of his body as well, even where had not received a steroid injection [21].

Study #2: a case report of FMT + hair regrowth in an elderly patient with diffuse alopecia areata

In a second study investigating FMT’s effects on an elderly man (86-year old) with diffuse alopecia areata, researchers found some unexpected benefits [15]. Originally, FMT was used to treat his intestinal disorders (with success). However, alongside the treatment of his other digestive ailments, his hair thickness began to return. What’s more, his previously gray hair had regrown as its original color.

These are just three case reports. That’s not really “overwhelming” evidence…

You’re right! We always have to evaluate any intervention in respect to its quality and quantity of evidence. In regard to FMT and alopecia areata, the quality and quantity of evidence is low: three uncontrolled, retrospective case reports.

Having said that, we also have to recognize that the total number of alopecia areata patients who (1) develop C. difficile, and (2) have it progress to the severity where they become eligible for an FMT – is also low. On that note, the evidence here has excited other research teams enough to launch a clinical trial on FMT and alopecia areata – the results of which will (hopefully) be available in the coming year.

So, needless to say, the preliminary evidence (and mechanistic data) supporting a connection between is FMT and AA-related regrowth is exciting enough to continue exploring.

How might FMT’s improve alopecia areata?

Alopecia areata is mainly categorized by an autoimmune attack on the hair follicles. This is predominantly mediated by a group of immune cell known as T-cells. Specifically, a type of T-cell known as TH17 [16].

Not surprisingly, TH17 is a major contributor to intestinal conditions that manifest as inflammation. Since the gut is our largest site of immune cell concentration, then by altering the gut microbiome to a more favorable anti-inflammatory profile, we may be able to alter T-cell activity throughout the rest of our body.

In fact, studies have shown that modulating the microbiome to favor this anti-inflammatory profile can nearly shutdown TH17 cell activity [17]. By this very same mechanism, it is possible that a more widespread shutdown of TH17 could alleviate a TH17-mediated attack on hair follicles – even at the top of the scalp.

Furthermore, there is an established link between inflammatory bowel disease and alopecia areata [18]. The implication: an unhealthy microbiome may drive both inflammatory bowel disease and alopecia areata. After all, patients with alopecia areata and inflammatory bowel conditions who undergo FMT seem to inadvertently regrow hair – and at a consistency worth noting by investigators.

Summary so far: Alopecia areata (AA) is an autoimmune form of hair loss; it’s likely driven by the over-activation of T-cells, and specifically, TH17 cells. Interestingly, patients with AA who’ve undergone stool transplants (FMTs) to treat C. difficile infections have inadvertently regrown hair. The gut microbiome is the body’s largest site of immune cell concentration – and thereby TH17 activation. So, it’s plausible that FMTs might dampen TH17 immune activation – all by restoring gut microflora balance to a more commensal state.

Telogen effluvium and stool transplants

Telogen effluvium (TE) is a temporary form of hair loss that is characterized by a dysregulation of the hair cycle.

This can occur in many ways: for instance, too many hairs can “shed” prematurely, or there can be a delay between when a hair sheds out and when a new hair grows in (to start a new hair cycle). This often presents as diffuse thinning, or sometimes even region-specific shedding (oftentimes the hairline for women).

A hair loss patient with suspected telogen effluvium (TE)

What causes telogen effluvium (TE)?

Telogen effluvium (TE) is sort of like a catch-all diagnosis for a wide array of hair loss triggers. But the main drivers of TE are often considered (1) stress (emotional or physical), (2) nutrient imbalances, and (3) chronic conditions (i.e., hypothyroidism, heavy metal toxicities, etc.).

Currently, there are no studies investigating a link between FMTs and TE. However, there is mechanistic evidence that FMTs may help address some (of the many) underlying factors leading to TE.

For example, nutrient deficiencies – namely, iron, zinc, and/or vitamin D – have been associated with telogen effluvium [20]. Given that evidence implicates the state of the microbiome in nutrient absorption, it’s possible that disruptions to the microbiome may result in poor nutrient absorption and, consequently, telogen effluvium-related hair shedding [21].

Research has also found elevated cadmium levels in some people with TE – a trace element that may trigger hair shedding if consumed in excness [22]. Most interesting, though, is that excessive cadmium has also been shown to alter the gut microbiome of mice in a way that directly mirrors individuals plagued by antibiotic-resistant Clostridium difficile infections… the exact condition FMT is designed to treat [23].

Altogether, direct (i.e., by bacterial infection) or indirect (i.e., by excess cadmium) changes to the microbiome, both of which seem to be associated with telogen effluivum, may benefit from FMT.

Summary so far: Telogen effluvium (TE) is a temporary form of hair loss caused by a disruption to the hair cycle – oftentimes resulting from stress, nutrient imbalances, or a chronic condition. While no evidence directly implicates stool transplants as a therapeutic procedure for TE, there is mechanistic data showing that our gut microbiome has the capacity to improve chronic conditions as well as the synthesis of vitamins commonly found as deficient in TE patients. Therefore, it’s possible that stool transplants might help TE by addressing its underlying causes. But again, we’re extrapolating here!

Androgenic alopecia and fecal transplants

Androgenic alopecia (AGA) is one of the world’s most common hair loss disorders – affecting at least 50% of women and 80% of men throughout a lifetime. Its often characterized by progressive hair follicle miniaturization, whereby affected hair follicles get thinner and thinner over a series of hair cycles. It presents most commonly across the top of the scalp as temple recession + a bald spot in men, and diffuse thinning in most women.

Androgenic alopecia in a male: temple recession

What causes androgenic alopecia (AGA)?

While all of the causes aren’t fully elucidated, most researchers agree that AGA is caused by a combination of male hormones and genetics, and possibly the scalp’s environment (i.e., inflammatory microorganisms, the contraction of muscles surrounding the scalp perimeter, inflammation-mediated tension, etc.).

Specifically, the hormone dihydrotestosterone (DHT) seems to overexpress in balding scalp regions. In vitro studies demonstrate that DHT may trigger premature shedding, inflammatory signaling proteins, and cell death in dermal papillae cells (the “powerhouse” of the hair follicle) – all of which can lead to progressive hair follicle miniaturization. Moreover, studies have shown that men without DHT do not go bald, and that reducing DHT can help prevent (and partially reverse) the balding process.

Is there evidence that stool transplants can improve pattern hair loss (AGA)?

Clinical evidence? No. Mechanistic evidence? Yes. Anecdotes of AGA improvements after stool transplants? Yes – even with photos. We’ll uncover all of this below.

First, to our knowledge, no case reports or clinical trials investigating the benefits of FMT have occurred. Nonetheless, the absence of evidence doesn’t imply evidence against a therapy (remember: FMTs are a very limited intervention). On that note, there are anecdotes online of people with AGA regrowing their hair (accidentally) following a fecal transplant.

One anecdote comes from a male forum user who suffered simultaneously from both irritable bowel syndrome (IBS) and AGA. In the past, he’d tried to treat his AGA with finasteride. Unfortunately, he did not see any improvements, so he stopped using the drug.

In search for a way to improve his IBS, he later stumbled upon the evidence supporting fecal microbiota transplants to treat C. difficile, Crohn’s disease, and gut dysbiosis. His symptoms were severe enough that he ended up tracking down a willing practitioner and giving the therapy a try – potentially outside of legal means.

A week after the therapy, he reported that his hair shedding dramatically decreased. A year later, he reported significant hair thickening (and potential regrowth)… regrowth that occurred outside of any drug interventions or hair growth therapies.

AGA-related hair regrowth one-year after a stool transplant

This anecdote is promising. But again, it’s just the experience of one person. Beyond this report, are there any other examples?

When it comes to fecal microbiota transplants – we couldn’t find any other anecdotes of hair regrowth from AGA. But interestingly, we were able to find reports of hair regrowth (with photos) from people adhering to incredibly restrictive diets that completely revamp gut microflora constitutions.

One such diet is the carnivore diet – whereby someone nearly completely restricts carbohydrate and fiber intake and begins to subsist entirely off of meat. It sounds like a crazy diet (and it just might be). However, it’s also the only diet where I’ve actually seen people regrow hair lost due to androgenic alopecia. For instance:

• A 1928 case report detailed two men under clinical observation for an entire year while eating only meat. One observation from the investigation team? One of the men saw a complete stop in the progression of his  pattern hair loss.
• Some members of our community (who have failed to see success with drugs like finasteride) have later opted to adopt the carnivore diet as an experiment for health. A few of these members have reported hair regrowth.

For an example – take Brian (a member of our community). He’d tried finasteride for two years, saw zero improvements, and then eventually quit the drug. Later, he and his wife decided to try the carnivore diet. Simultaneously, he also started to incorporate our scalp massages to see if that would improve his hair loss (since finasteride didn’t work).

One year later, he’d noticed significant hair regrowth at hairline, as well as overall hair thickening. Here were his results.

AGA-related hair regrowth one-year after the carnivore diet + massaging

Interestingly, preliminary evidence suggests that the carnivore diet may increase gut microorganism biodiversity – one of the objectives of FMT. It may also reduce the totality of bacteria inside the gut – since these microorganisms feed off carbohydrate and fiber (two things that are nearly eliminated on a diet consisting of all meat).

Moreover, the carnivore diet eliminates a lot of inflammatory food groups (i.e., FODMAPs) that might contribute to systemic inflammation for sensitive individuals. This may help reduce the number of pathogenic bacteria residing in the gut, as well [27].

This leads to some interesting discussion points about a possible connection between AGA, stool transplants, the carnivore diet, and subsequent changes to the microbiome that could improve hair loss outcomes. We’ll explore these below.

Mechanisms: how might stool transplants improve pattern hair loss?

There’s evidence that our microbiome may help regulate our endocrine system (i.e., the balance of our sex hormones). More specifically, our microbiome may play a direct role in the metabolism of androgens – the sex hormone implicated in AGA.

To start, here’s a quick overview on how hormone metabolism works:

1. Once circulating hormones have “completed” a task, they reach the liver. The liver is where free hormones (i.e., the active, unbound hormones) in our blood are processed to later become excreted.
2. The liver conjugates these free hormones. Simply put, the livers converts the structure of these hormones from lipophilic (i.e., fat-loving) to hydrophilic (i.e., water-loving). This does two things: it makes the hormone less potent, and it increases that hormone’s chances of entering the digestive tract (i.e., small and large intestine) where they can get excreted.
3. Once these conjugated forms of hormones enter the digestive tract, the body excretes these conjugates or metabolites in the stool and urine.

Put simply, our liver conjugates active hormones, those hormones enter our digestive tract, then our digestive tract flushes those hormones out of the body.

But here is where things get interesting: some of our gut bacteria produce an enzyme called beta-glucuronidase. This enzyme has the ability to reverse the process of hormone excretion. Specifically, when conjugated forms of hormones come into contact with beta-glucuronidase, those hormones become unconjugated. In other words, they reconvert back into an active (i.e., unbound) form – where they can potentially reenter our circulatory system.

So, if gut bacteria have the ability to act as gatekeepers for hormone excretion and reabsorption, what does this have to do with AGA?

Fascinatingly, research in healthy men has demonstrated that free dihydrotestosterone (DHT) – the hormone implicated in AGA – exists at levels in the colon at levels 70-fold higher than free DHT found in the blood [24].

This suggests (at least) two things:

1. Serum levels of DHT represent just a tiny fraction of total DHT within our body.
2. If this free DHT can exit the digestive tract and reenter the circulatory system, this means that gut bacteria might act as a gatekeeper for androgen excretion / reabsorption… and that our microflora might be directly implicated in androgenic-linked conditions: heart disease, prostate enlargement, and maybe even pattern hair loss.

It’s already been shown that gut bacteria have a directly influence on steroid levels. In fact, in the case of periodontal disease and gingivitis, certain cultured bacterial species can actually increase levels of testosterone and DHT [25]. Moreover, researchers have linked this increase to the development of inflammation in periodontitis itself.

Free DHT (as opposed to conjugated DHT) is the type of DHT that likely elicits the majority of DHT-mediated effects on the body. This includes supporting the processes that lead to AGA. You can learn more about this here.

Can unconjugated DHT (in the gut) reenter the circulatory system?

No studies have demonstrated this. But to our knowledge, no studies have actually asked this question (to our knowledge). Not to sound like a broken record, but the absence of evidence cannot imply evidence against something.

It’s worth noting that gut bacteria can produce (and recirculate) estrogens. So, it’s not out of the realm of possibilities that DHT can also be recirculated. In fact, it’s more likely than not.

Moreover, studies on patients with post-finasteride syndrome (long-lasted sexual dysfunction and/or cognitive disorders after cessation of finasteride) show marked gut microbiota alterations [26]. Researchers believe that these microbiota alterations may possibly contribute to the symptoms of finasteride syndrome.

Of course, there are still no clear connections between post-finasteride syndrome and these microbiome alterations. However, if free DHT levels in the colon contribute to overall DHT levels and finasteride results in prolonged changes to the population of these bacteria, it’s possible that reduced colon DHT may contribute to blood DHT, and, thereby the symptoms of post-finasteride syndrome.

Similarly, the opposite could also prove true: if colonic DHT influences blood DHT levels (in an upwards or downwards direction), then anything that increases the total number of our gut bacteria might also increase DHT levels.

Whether this affects scalp DHT (and thereby AGA) – we just don’t know. But we do find these anecdotes of stool transplants and/or carnivore diets regrowing hair absolutely fascinating. After all, both interventions likely lead to improvements in gut biodiversity and changes to the total number of commensal / pathogenic microflora. Therefore, they likely alter DHT activity in the gut. But whether these effects extend to our scalp hair – we can’t yet say (aside from admiring those before-after photos and “hoping” that, after all these years, it’s just that easy to reverse AGA).

Summary so far: Androgenic alopecia (AGA) is driven by a combination of genes and androgens. Interestingly, some patients who’ve undergone stool transplants have later reported hair thickening from AGA without any other treatments. The main hormone implicated in AGA is dihydrotestosterone (DHT). Recent research has found that gut bacteria can actually produce DHT, and even convert it from an inactive to active form. Moreover, researchers recently discovered that free DHT is found in stool samples at levels 70-fold greater than in the blood supply. It has been demonstrated that gut microorganisms influence estrogen production, and the amount of estrogen circulating in our blood. Therefore, it’s not unreasonable to assume that gut flora may also act as gatekeepers for DHT activation between the gut and the circulatory system. If true, this may directly implicate gut bacteria in the pathogenesis of AGA.

Fecal microbiota transplants: undergoing the procedure

What’s it like to do a fecal microbiota transplant?

While FMT may sound like a cure-all for all autoimmune ailments, it’s worth mentioning that research here is still in its infancy, and there’s always the very real possibility that a transplant won’t work or might worsen your symptoms due to unforeseen interactions between donor and recipient microflora.

In the US and Europe, strict guidelines are set to screen a potential donor for any negative attributes that could trigger unwanted side effects for the recipient. There is a questionnaire that is given, stool sample analysis is performed approximately four weeks prior, and blood samples taken [1], followed by an additional interview at the time of the donation. Preferably, you would want a stool sample from someone close to you, with whom you may have shared a common environment. This reduces the chances of any unwanted immune reactions that may occur.

Any failure in the proper preparation of the FMT can present with complications such as bacteremia (i.e., bacteria in the bloodstream) or hospitalizations. Other mishaps such as perforations can occur, but tend to be attributed to the tools and technicians rather than infectious agents [10].

Usually, preparations of the fecal material are done up to six hours before the procedure. The sample is frozen, then thawed out, and, finally mixed with a solution to deliver in a syringe.

It’s also been shown that the size of the sample matters dramatically. Usually, sample sizes are around 50g, which is no more than a few teaspoons. With difficult to treat clostridium infections, larger sample sizes have demonstrated better efficacy and reduced chances chances of failure with the treatment [11]. Many times, FMT requires multiple treatment sessions as well for optimal results.

An important (and interesting) aspect of the procedure is the fact that antibiotics are not to be given to the recipient within 48-hours [12]. While this may seem like an obvious aspect of FMT, this also points to the possibility that it actually is the bacteria present within the stool itself that produces results… not another confounding variable such as immune molecules, proteins, or other components.

Even more supportive of that notion: studies have shown when the procedure is given to the lower digestive tract, (which is also where a majority of the gut microbiome resides), results are drastically better than when administered in the upper digestive tract [1].

Is there a way around the “yuck factor” of FMT?

The idea of taking someone else’s fecal material and implanting it inside of your colon isn’t exactly appealing. And while a lot of the hesitancy is likely psychological, it’s reasonable to ask if there’s a way to do an FMT without doing an enema.

Yes. Researchers have shown that oral capsules produced results on par with the procedure itself – at least in the treatment of resistant Clostridium infections [13]. Obviously, oral supplementation may come across as even less appealing to some. Tto others, the possibility of supplementation certainly reduces the “barrier to entry”.

Summary: stool transplants for hair loss

By regulating the gut microbiome and reducing gut inflammation, a fecal microbiota transplant may improve hair loss outcomes for alopecia areata, telogen effluvium, and perhaps even androgenic alopecia.

Evidence on stool transplants and hair regrowth is incredibly limited. Our knowledge base comes from:

• Four case reports demonstrating significant hair regrowth across patients with autoimmune forms of hair loss
• Anecdotes from people who’ve undergone stool transplants for gut dysbiosis and later reported inadvertent hair regrowth
• Mechanistic data revealing possible connections between stool transplants, the gut microbiome, DHT production, and immunological changes – as well as their overlap with common hair loss disorders.

Nonetheless, I personally find this arena of research fascinating, and I hope it rapidly expands.

In the meantime, please note that we’re not recommending stool transplants as a first-line of defense for any hair loss disorder. If you’re interested in getting one, you’ll need to connect with a qualified physician – we’re not in a position to help you here.

You can reach us in the comments any time!