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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

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. 

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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

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.

 

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

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!

Vitamin B1 – also known as thiamin (or thiamine) – is part of the B-vitamin complex. Marketers claim that vitamin B1 can help support healthy hair growth, reduce hair shedding, and even prevent hair loss. Then again, marketers also make the same claims about B-vitamins like biotin, niacin, and vitamin B12. And typically, the claims are just plain wrong.

So, is vitamin B1 any different? In this article, we’ll dive into the evidence (and answers).

First, we’ll uncover why some people that vitamin B1 helps support hair growth. Then, we’ll dive into the evidence on the vitamin B1 / thiamin-hair loss connection. Finally, we’ll dive into evidence that might implicate vitamin B1 as an accelerator of hair loss… and steps to take if you suspect you’re deficient.

By the end, you’ll have a better idea of whether vitamin B1 is a worthy investment for your hair, or just another marketing gimmick. If you have any questions or comments, please post them below!

What is Vitamin B1?

Vitamin B1 (also thiamin or thiamine), is one of the many members of the B vitamin family.  

Vitamin B1/thiamine

Researchers first identified this essential micronutrient through the study of beri beri, a serious disease of the nervous system that was common in South East Asia prior to the 1900s.

Unlike most diseases in that time, beri beri was much more common among wealthy citizens than it was among poorer citizens. Upon further investigation, researchers found the reason for the perplexing discrepancy was actually attributed to the differences in rice consumption. 

While poorer individuals tended to consume brown rice, richer individuals tended to consume milled white rice — devoid of the husks, bran, and germ.

Through experimentation with this brown rice, a Polish biochemist, Casmir Funk, was able to isolate the compound that prevented beri beri. This compound? He termed it thiamine, meaning sulfur-containing amine — what we now know as vitamin B1.

Fast forward to today: we now know that vitamin B1 plays a crucial role in mitochondrial health, metabolism of macronutrients, and energy production — processes that are essential for the normal functioning of almost every cell in the body (1).

But, beyond the prevention of serious neurological conditions, does vitamin B1 have any benefit to our hair? 

Let’s explore the evidence.

Vitamin B1: might it help support hair growth?

There’s no doubt that vitamin B1 is critical for important processes, like (1):

• The production of ATP, the energy molecule that fuels cellular activity
• The synthesis of amino acids
• The creation of NADPH, a co-factor necessary for steroid hormone production, fatty acid synthesis, and more.

And similar to other B-complex vitamins, vitamin B1’s role in these processes often form the basis of the claim that vitamin B1 can influence hair loss. After all, if you can’t produce amino acids — the raw material our hair is actually made of — how can you grow hair?

But, is this actually true? Are there any other ways that B1 might influence our hair? And what does this mean in the context of diet in the developed world?

Let’s explore the evidence.

Does a thiamine / vitamin B1 deficiency cause hair loss?

Maybe. But this isn’t the right question to ask. Rather, we need to ask this question in two parts:

1. Does a vitamin B1 deficiency cause hair loss?
2. Does a vitamin B1 deficiency within realistic parameters cause hair loss?

Why would we do this? Because at the extremes, almost anything causes hair loss. For instance, a “water deficiency” can cause hair loss. If we don’t drink water, we die. If we’re dead, we can’t grow hair. But that doesn’t mean that drinking water will regrow our hair. It also doesn’t mean we should warn people that hair loss is a side effect of a water deficiency.

The truth is that these types of logic leaps are what marketers use to claim that deficiencies in selenium, vitamin E, and iodine can all cause hair loss. Yes, this is true – but only if our scope of deficiency includes the endpoints: malnourished poverty-stricken children, people with genetic disorders who can’t absorb these nutrients, and people with certain chronic conditions that make nutrient assimilation nearly impossible.

All this is to say that we should ask if a thiamine deficiency, in the absolutes, causes hair loss. But the better question is: does a thiamine / vitamin B1 deficiency within realistic parameters cause hair loss, too?

Let’s take these one-by-one.

1. Does a thiamine deficiency, at the extremes, cause hair loss?

Maybe (in rodent models).

This 1968 study (2) sought to determine what happens in mice fed a diet that rapidly induces a thiamine deficiency. After two and a half weeks, some mice began to experience rapid weight loss, followed by abnormal hair shedding. Soon thereafter, neurological function began to decline. After four weeks, the mice were confused and could barely walk – symptoms similar to those seen in humans with beri beri.

However, it was unclear if the hair loss was caused by the vitamin B1 deficiency or the rapid weight loss.

2. Does a thiamine deficiency, within realistic parameters, cause hair loss?

Probably not.

For starters, people with beri beri rarely reported hair shedding (even despite their rapid weight loss). Moreover, when we expand our scope to human studies, we haven’t found any hard evidence that causally links a vitamin B1 deficiency to hair loss.

We could close the case right there, and say the article is done. At the same time, the absence of evidence doesn’t always imply evidence of absence.

For instance, there’s always the possibility that vitamin B1 might exacerbate certain chronic conditions linked to hair loss, or certain disease states associated with shedding disorders.

In fact, we could assert that since a vitamin B1 deficiency can lead to rapid neurological decline and thereby weight loss, and because rapid weight loss can trigger excessive (but temporary) hair shedding, then vitamin B1 deficiencies might be indirectly related to hair loss. The deficiency causes the weight loss; the weight loss causes the hair loss.

But again, if you’re so deficient in vitamin B1 that you start losing weight, you’ve got bigger things to worry about than your hair (like rapid impending neurological deterioration).

So, do we see any other circumstances where vitamin B1 is indirectly linked to hair shedding or hair loss?

Potentially. We can find them by look at the role of vitamin B1 in the body, and then comparing this to how different types of hair loss actually develop.

Vitamin B1 deficiency may exacerbate autoimmunity

At present time, there have been several animal studies conducted to investigate a link between vitamin B1 and autoimmunity. In general, these studies have suggested that vitamin B1 deficiencies may exacerbate autoimmunity in certain autoimmune disorders – specifically, multiple sclerosis (3, 4). It stands to reason that improving vitamin B1 deficiency may also improve these autoimmune conditions.

So, how could these effects translate to hair loss?

There are several forms of hair loss that seem to be mediated by autoimmune processes. These include alopecia areata as well as some forms of scarring alopecia.

If thiamine deficiencies happened to exacerbate the autoimmune processes involved in these hair loss disorders, it’s possible that restoring thiamine levels could improve these conditions.

Again, there’s no evidence that vitamin B1 deficiency is related to these hair-related autoimmune conditions. And while all autoimmune conditions involve autoimmune processes, not all autoimmune conditions develop in the same way. Thus, we can’t necessarily extrapolate the results from the animal studies, which primarily looked at multiple sclerosis, to the autoimmune conditions that lead to hair loss.

There’s also another point to consider: the effects of certain compounds reflected in animal studies are also traditionally very difficult to extrapolate to humans. Take our rodent study from earlier: thiamin-deficient rodents developed weight loss, neurological decline, and hair loss; whereas humans with beri beri – a sign of a thiamin deficiency – typically only develop weight loss and neurological decline.

That leaves us with one last piece of evidence to consider when it comes to linking autoimmune hair loss to vitamin B1: a case series on three human patients with autoimmune thyroid conditions (5).

Vitamin B1, autoimmune thyroid disorders, and hair shedding: a possible connection?

Autoimmune conditions that affect the thyroid – like Graves’ disease and Hashimoto’s thyroiditis – can have a domino effect on hair growth which is, in part, controlled by thyroid hormones. When these hormones get too high (i.e., Graves’ disease) or too low (i.e., Hashimoto’s thyroiditis), it can cause telogen effluvium – a form of diffuse hair shedding.

Interestingly, vitamin B1 might have relevance here, especially in the context of Hashimoto’s thyroiditis.

In one case series, doctors administered vitamin B1 to three patients with Hashimoto’s thyroiditis. They hypothesized that vitamin B1 could help relieve one of the hallmark symptoms of low thyroid hormone: fatigue. 

Amazingly, that’s exactly what vitamin B1 did. In just a few hours to a few days, administration of B1 drastically improved the patients’ fatigue. 

But, this wasn’t because of a subsequent improvement in the underlying autoimmune condition.

Instead, the authors hypothesized that the autoimmune processes involved in Hashimoto’s thyroiditis may have resulted in a vitamin B1 deficiency, subsequently leading to a reduction in energy production and, thus, fatigue.

In other words, the vitamin B1 deficiency likely isn’t a contributor to the development of Hashimoto’s thyroiditis. Instead, vitamin B1 deficiency, in this case, is a consequence of the condition.

As such, we can’t expect vitamin B1 to actually improve Hashimoto’s thyroiditis or the hair loss that occurs as a result. Instead, vitamin B1 can only improve symptoms related to a vitamin B1 deficiency that may occur alongside the condition.

So, we’ve established that vitamin B1 may or may not improve autoimmune forms of hair loss. We’ve also ruled out vitamin B1 as a means to improve Hashimoto’s thyroiditis and the hair shedding that ensues as a result.

But, are there any other pathways by which B1 might influence hair loss? Maybe… and that leads us to point number two.

Vitamin B1 deficiency may impair glutathione synthesis

Glutathione is a sulfur-containing compound with powerful antioxidant activity. Unlike antioxidants we consume in our diet (like polyphenols in green tea, berries, and other health-promoting foods), glutathione is manufactured by our own cells from amino acids like cysteine, glycine, and glutamic acid. This process requires NADPH, which requires vitamin B1 (along with various other B vitamins) (6).

So, how does this relate to hair loss?

Glutathione deficiency is associated with many conditions including diabetes, cardiovascular disease, as well as autoimmune diseases (7). Some studies also show low glutathione is associated with androgenic alopecia (AGA) (8).

As an anti-inflammatory agent, it’s possible that glutathione deficiency could exacerbate the microinflammation in AGA follicles — a process that drives the hair loss observed in AGA (7, 9). 

In this context, it’s possible that through a possible increase in glutathione, vitamin B1 could reduce inflammation in AGA and, thus, improve AGA.

But there’s a difference between possible and plausible. Yes, if we stretch our imagination, it’s possible that a vitamin B1 deficiency might decrease glutathione production, and that if enough of this occurs in balding hair follicle sites, this decrease might exacerbate inflammation in AGA.

Possible, yes. But plausible?

Probably not.

While B1 deficiency seems to be related to low glutathione levels, vitamin B1 deficiency is extremely rare amongst most of the population. So, in this context, vitamin B1 is probably not something that most AGA patients need to worry about.

In these cases, glutathione deficiency is more likely to be related to co-morbidities seen in AGA: conditions like diabetes, obesity, and cardiovascular disease (all of which we know can deplete glutathione) (10).

So, while vitamin B1 deficiency could, technically, lead to or exacerbate a glutathione deficiency, it’s safe to say this is probably not the case for most AGA patients with low glutathione.

A quick recap

So far, we’ve established that B1 is an essential micronutrient. We’ve also established that in its complete absence, it can cause hair loss in rodents. Aside from that, it doesn’t appear that a vitamin B1 deficiency is a major driver of hair loss in humans.

The reason for this is three-fold: 

• Vitamin B1 deficiency is extremely uncommon in the general hair loss population.
• In the rare cases where vitamin B1 levels are depleted and associated with hair loss, improving vitamin B1 levels only improves symptoms associated with vitamin B1 depletion. In other words, vitamin B1 improves nervous system abnormalities like fatigue but not the underlying conditions that lead to hair loss.
• When looking at the relationship between vitamin B1, glutathione, and AGA, it’s unlikely that vitamin B1 deficiency contributes to low glutathione levels that may exacerbate hair loss. Rather, low glutathione levels observed in some patients appear to be a consequence of some common co-morbidities associated with AGA. 

So, that leads us to this conclusion: in the overwhelming majority of cases, vitamin B1 is not likely to confer any benefit in hair loss.

This leaves us with one last question worth asking before we close the books on the vitamin B1-hair health connection…

Could increasing vitamin B1 levels beyond normal levels have any negative effect on hair loss?

Maybe, maybe not. Let’s look at the research.

Why vitamin B1 might be bad for hair: the NADPH-DHT connection

Vitamin B1 is an essential cofactor in the production of the molecule, NADPH.

NADPH – or nicotinamide adenine dinucleotide phosphate – is a cofactor for enzymatic reactions. In other words, it’s a molecule that helps kickstart processes in the body. Earlier we established that NADPH was crucial for glutathione production. But that’s not all that NADPH does. NADPH is also essential for the production of steroid hormones.

Specifically, NADPH is a key molecule of the enzymatic process that converts testosterone into dihydrotestosterone, or DHT. Without NADPH, the enzyme that performs this conversion cannot function (11).

So, what does this mean for hair?

If you’ve done any research into androgenic alopecia (AGA), you probably already know that DHT is a significant contributor to the development of pattern hair loss (12). As such, any increase in DHT conversion could potentially worsen or speed up the balding process.

But, this would require NADPH to increase beyond what’s considered “physiological” — or what’s considered normal. So, does vitamin B1 do this?

Probably not. But we just don’t know.

What we do know is that, oftentimes, enzymes that produce molecules like NADPH have negative feedback mechanisms in place. This means that when their end-products increase, the body automatically reduces the activity of the enzymes that produce them. The net product is no increase in production.

However, this isn’t always the case. In some cases, these negative feedback loops are dysfunctional.

So, it’s possible that vitamin B1 doesn’t increase NADPH beyond what’s considered normal. As such, it’s also possible that vitamin B1 has no impact on DHT levels. At the same time, it’s also possible that it could.

In either case, the solution is the same: leverage diet to ensure vitamin B1 sufficiency and address a vitamin B1 deficiency if it’s present — but don’t go overboard.

If we’re deficient in B1, what should we do?

It’s important to note that an overwhelming majority of individuals likely aren’t deficient in vitamin B1. But, that doesn’t mean it’s impossible. Of the small pool of individuals B1 deficiency seems to affect in the modern world, risk factors appear to be:

• Hashimoto’s thyroiditis (5)
• Gastric bypass surgery (13)
• Anorexia (13)
• Severe crash dieting (13)
• Marked impairments in nutrient absorption, as in severe inflammatory bowel disease (13)
• Alcoholism (13)
• Septic shock (14)

But, again, it’s important to underscore that, even in these cases, we shouldn’t expect vitamin B1 to regrow our hair. This is because a vitamin B1 insufficiency is highly likely to present alongside other contributors to hair loss – like low thyroid hormone, zinc deficiency, iron deficiency, and severe calorie deficit. So, an improvement in B1 levels alone isn’t going to override these other factors. If anything, the thiamine deficiency-hair loss connection is more association than it is causation.

In any case, maintaining sufficient vitamin B1 levels is essential for overall health. So, you should aim to hit the recommended daily intake (RDI) everyday.

The good news is that you’re probably already doing this without even thinking about it – especially with all of the B-complex fortified foods out there. And if you find yourself falling into any of the risk categories, it’s not hard to find a supplement containing thiamine; nearly every multivitamin includes it as an ingredient.

At the same time, there could be a small minority of B1 deficiencies that go undetected, as was the case with the case series of Hashimoto’s thyroiditis patients. So, if you find yourself with fatigue that isn’t responding to standard treatment for Hashimoto’s thyroiditis, it may be worth discussing the possibility of vitamin B1 supplementation with your doctor.

Summary 

Vitamin B1 is an essential vitamin. It ensures our body can effectively produce amino acids, glutathione, and other cofactors that are crucial for cellular function.

Deficiencies in vitamin B1 have been linked to weight loss, neurological decline, and hair loss in rodents. In humans, the evidence points more so toward neurological decline and weight loss than it does hair shedding. Having said that, a vitamin B1 deficiency might indirectly exacerbate hair loss through:

1. Rapid weight loss
2. Autoimmunity
3. Glutathione impairment

But the bottom line is this: if your thiamine / vitamin B1 levels are low enough to associate with hair loss, you’ve got bigger problems than hair… like mental debilitation, neurological deterioration, and impending death.

Needless to say, 99.9% of us probably don’t need to be supplementing with vitamin B1 as a hair loss preventive. In fact, given vitamin B1’s relationship to NADPH production, and NADPH’s relationship to DHT, we could make a similar logic-leap argument that too much vitamin B1 may exacerbate hair loss.

This leaves us with one firm conclusion: maintain sufficient vitamin B1 levels by consuming the recommended daily intake. In the developed world, nearly every single diet will do this for you… provided you don’t have any of the hallmarks that increase your risk of a B1 deficiency (i.e., alcoholism, gastric bypass surgery, anorexia, etc.).

In the rare case that you are deficient, work with a doctor to address why your levels might be decreased in the first place and, if needed, to increase your levels with supplementation.

Have any questions about Vitamin B1 and hair health? Please leave them below in the comments!

The calcium-hair loss connection

The connection between calcium and hair loss isn’t straightforward. On the one hand, no studies have directly examined the relationship between calcium and hair loss. On the other hand, calcium imbalances are common in chronic conditions linked to hair shedding. So, what’s the verdict on the calcium-hair loss connection?

Can low calcium levels cause hair loss? What about high calcium levels? And if yes, by which mechanisms?

This article uncovers the answers. By the end, you’ll uncover:

• The calcium-hair loss connection: where this mineral does (and doesn’t) influence hair loss
• Calcium loading: why supplementing isn’t always the answer
• The two chronic conditions linked to hair loss and a calcium imbalance… and what to do about them.

If you have any questions, please feel free to reach out in the comments.

What is calcium?

Calcium is one of the most abundant trace minerals in the body. It’s most well-known for its role as a building block of teeth and bone. But, calcium does much more than that. It’s a cellular signaling molecule – driving processes from inflammation to skin cell production and the firing of our neurons (1-3).

Calcium: an essential mineral

Interestingly, calcium also influences our endocrine system: the glands, tissues, and organs that regulate hormone production. And our endocrine systems can influence nearly every aspect of biology, including the development of common hair loss disorders like androgenic alopecia (AGA) and telogen effluvium.

This is why so many people wonder if calcium plays a role in hair loss. The thinking is as follows: calcium levels influence our hormone production, and hormones influence hair loss. So maybe calcium imbalances can cause hair loss.

But is this actually true? Let’s dive into the evidence.

Can a calcium deficiency cause hair loss?

Necessary disclaimer: at the extremes, anything can cause hair loss. For example, a water deficiency can cause hair loss. If we don’t drink water, we die. If we’re dead, we can’t grow hair.

The same is true for most vitamins, minerals, and nutrients – including calcium. If we don’t ingest any calcium, we can’t grow bone. If we can’t grow bone, we die. If we’re dead, we can’t grow hair.

I hope you see where I’m going with this – which is that we’re asking the wrong question. Rather than ask, “Can a calcium deficiency cause hair loss?”, we need to ask is, “Can a calcium deficiency within realistic means cause hair loss?”

And to answer that question, we have to dive into the literature. So, what do the studies say about calcium’s role in hair loss?

There are no studies measuring calcium’s role in human hair loss.

We know that calcium is essential for the function of many tissues. We know that calcium plays a significant role in cellular signaling, a process necessary for maintaining hair growth. And we know that, in animal studies, vitamin D-deficient dogs fed a low-calcium diet develop hair loss (4).

Unfortunately, no studies have directly examined the relationship between calcium and hair loss in humans. That means we don’t yet have data to directly answer this question.

What also makes this complicated: calcium is a tightly regulated mineral. We need calcium to mediate thousands of biochemical processes. In cases of dietary deficiencies, our bodies pull calcium from bone to maintain optimal levels. In cases of dietary surpluses, our bodies expel excess calcium to avoid over-accumulation.

For these reasons, it’s unlikely that – under normal settings – our bodies would let calcium levels to drop low enough to cause problems like bone mineral depletion or hair cycling dysfunction.

But what about abnormal settings?

For example, what about in cases of disease states where our bodies’ nutrient demands are much higher… or nutrient absorption is much lower (i.e., SIBO)… or certain supplements, medications, or surgeries have caused a dysregulation of nutrients in the body?

Under these scenarios, are calcium levels implicated in hair loss? Interestingly, the answer is yes.

Both low and high calcium levels are linked to hair loss – at least indirectly. Here’s how.

The indirect links between calcium imbalances & hair loss

Calcium deficiencies: polycystic ovarian syndrome (PCOS)

Polycystic Ovarian Syndrome (PCOS) is a chronic condition that affects 15-20% of women of reproductive age (5). Its biological biomarkers: high testosterone and insulin insensitivity. Its tell-tale signs: the formation of small cysts on the ovaries, missed or infrequent periods (cycles of 35+ days), weight gain, sluggishness, and even the development of female pattern hair loss – a consequence of the prolonged hormonal imbalances (specifically, the elevated testosterone).

Interestingly, PCOS is also associated with slight (but significant) deficiencies in vitamin B-12, C, D, and calcium (6). This begs the question: are these nutrient deficiencies a cause or a consequence of PCOS?

At least so far, literature reviews suggests that PCOS-related nutrient deficiencies are consequences of PCOS, not causes (7). Specifically, these nutrient deficiencies are partly the result of prolonged insulin resistance, which can increase nutrient demand.

That means that calcium deficiencies do not cause PCOS, and are thereby only indirectly associated with the female pattern hair loss that often accompanies the condition.

Calcium surpluses: hyperparathyroidism

Interestingly, there’s at least one more way that calcium imbalances are indirectly linked to hair loss. In this case, it’s a calcium surplus… and the condition is called hyperparathyroidism.

To explain this, we’ll start by uncovering the parathyroid glands, how this relates to hair shedding, and where calcium comes into play.

The parathyroid-hair loss connection

The parathyroid glands are part of our endocrine system. They consist of four glands that sit right behind the thyroid.

When our blood calcium levels go down, the parathyroid is responsible for getting them back in the normal range. It does this by secreting a hormone called parathyroid hormone (8).

The way this happens is out-of-scope for this article, but in short, parathyroid hormone signals for our bodies to leech calcium from our bone. In leeching bone calcium, blood levels of calcium increase, and the calcium then gets redistributed to other tissues in need.

Parathyroid’s action on bone to maintain calcium homeostasis

However, there are cases where this process can backfire.

Studies have shown that when parathyroid hormone is added to hair follicle cultures, it can cause them to prematurely enter the catagen phase of the hair cycle (9). Catagen is the transition step between the growth and shedding phases of the hair cycle. Therefore, anything that initiates catagen will eventually culminate into hair shedding.

If many hairs enter catagen at once, the hair shedding can be so drastic that it leads to a visible decrease in hair density. This can lead to a temporary form of hair thinning called telogen effluvium.

Hypothetically, this opens up the possibility that chronically elevated parathyroid hormone levels could trigger chronic, persistent hair shedding. Unsurprisingly, hair loss is a common complain amongst those with an overactive parathyroid (9).

So, what causes parathyroid hormone to remain elevated for significant periods of time? And what does any of this have to do with calcium intake?

The parathyroid-calcium connection

When parathyroid hormones go out of range, it is classified as a condition called hyperparathyroidism. There are two types of hyperparathyroidism: primary and secondary.

Primary hyperparathyroidism is almost always caused by a tumor on the parathyroid gland (10). Treatment for this type of hyperparathyroidism is usually confined to removing the affected gland – and through surgery.

Secondary hyperparathyroidism, on the other hand, are characterized as out-of-range parathyroid hormone levels caused by something unrelated to a direct dysfunction of the parathyroid gland itself. As such, its causes are more complex, individualized, and wide-ranging than primary hyperparathyroidism. 

One common cause of secondary hyperparathyroidism is chronic kidney disease – which severely impacts the kidney’s ability to handle calcium and vitamin D.

The other common cause of secondary hyperparathyroidism is a vitamin D deficiency (11). Interestingly, vitamin D helps regulate calcium levels in the blood. When vitamin D levels are low, calcium levels in the blood drop. This engages the parathyroid gland to increase secretion of parathyroid hormone, all so that calcium levels can increase.

Low vitamin D >> low serum calcium >> increased parathyroid hormone >> increased calcium leeching from bone >> increased serum calcium

Therefore, hyperparathyroidism is another scenario where we can see imbalanced calcium levels and hair loss. In this case, it’s usually high calcium. But similar to PCOS, the calcium dysregulation is a consequence of the chronic condition, and not a cause of the hair thinning.

If I have secondary hyperparathyroidism, will eating less calcium lower my calcium scores?

Probably not. Here’s a quick overview of the relationship between calcium intake and elevated parathyroid hormones:

• No studies have currently established a link between calcium and secondary hyperparathyroidism. 
• One study on almost 60,000 women found that increased calcium intake was independently associated with a decreased risk of developing primary hyperparathyroidism (12). This suggests that, in the long run, consuming adequate calcium may prevent primary hyperparathyroidism caused by tumors.
• Outside of this, some studies (13-15) have suggested that calcium and parathyroid hormones have an inverse relationship. In other words, decreased calcium intake may lead to increased parathyroid hormone levels while increased intake leads to lower parathyroid levels. However, this increase doesn’t lead to parathyroid hormones going out of range.

From this, we can glean three things: (1) adequate calcium intake may prevent primary hyperparathyroidism, but (2) poor calcium intake doesn’t appear to cause secondary hyperparathyroidism, and (3) decreased calcium intake may lead to increased parathyroid hormone (however, this doesn’t likely lead to hyperparathyroidism).

So, when we look at the big picture, it seems that poor calcium intake isn’t strongly associated with hyperparathyroidism as both a cause or a treatment. Rather, it elevates parathyroid levels, but not too far outside of the normal range.

Therefore, if you’re dealing with hair loss and you have high (or low) calcium scores, consider getting tested for vitamin D, PCOS, and hyperparathyroidism. In the interim, make sure to eat adequate amounts of calcium.

The good news is that for most modern diets, getting enough calcium shouldn’t be too hard.

How to optimize calcium intake

In general, I’ve always felt best to get nutrients from foods as opposed to supplements. In the case of calcium, this is especially important. Here’s why.

Calcium supplementation has been linked to an increased risk of cardiovascular events (16). In some cases, calcium supplements can also disrupt the pH of the stomach, which is critical for optimal digestion and nutrient assimilation (and, thus, hair growth) (17).

The good news is that calcium is readily available in the diet – even if you’re not currently consuming dairy. Here are just a few non-dairy foods replete with calcium:

Food sources of calcium (RDI: 1,000mg)
Food source, serving size	Mg, % DV
Egg shells (3g)	1,200mg, 120%
Firm tofu (100g)	683mg, 53%
Black eyed peas (100g)	128mg, 10%
Okra (100g)	77mg, 6%
Trout (100g)	86mg, 7%
Acorn squash (100g)	44mg, 3%

For most adults consuming a balanced diet, you’re probably getting enough calcium. However, if you want to be sure about your calcium intake (and other nutrients), you can always track the micronutrient sufficiency of your diet using Cronometer or FitDay.

Summary

Calcium is an essential nutrient. But aside from extreme deficiencies, calcium imbalances don’t appear to cause hair loss.

There are no human studies examining the role of calcium levels and hair loss. However, calcium is indirectly related to hair follicle cycling. Moreover, studies have shown that vitamin D-deficient animals fed a low calcium diet develop alopecia. Therefore, it’s not unreasonable to wonder if calcium plays a role in hair loss.

To date, there are only two scenarios where calcium imbalances are linked to thinning hair:

1. Low calcium and hair loss observed in polycystic ovarian syndrome patients
2. High calcium and hair loss observed in hyperparathyroid patients

But in both situations, the calcium imbalances are consequences of the condition, rather than the cause of the hair loss.

Evidence shows that dietary calcium has little-to-no impact on blood calcium levels, at least within normal boundaries. Having said that, calcium supplementation may lead to an increased risk of heart disease – and potentially as a direct consequence to increased arterial calcification. For these reasons, it’s generally best to avoid calcium supplements altogether and stick to food sources (if possible).

The bottom line: calcium likely plays little to no role in the overwhelming majority of hair loss cases. If you’re dealing with hair loss and you have high (or low) calcium scores, consider getting tested for vitamin D, PCOS, and hyperparathyroidism. You might save yourself a lot of time, energy, and hair.

Questions? Comments? Please reach out in the comments section below.

Does vitamin B12 improve hair growth? Supplement companies say yes, but scientific studies reveal a much murkier (and nuanced) relationship between vitamin B12, hair loss, and hair growth… one you’ll want to understand before you start supplementing.

In this article, we’ll dive into the arguments for and against a connection between vitamin B12 and hair growth. We’ll explore methylation, vitamin B12’s role in the hair cycle, and B12’s connection to different hair loss disorders. Then, we’ll reveal when vitamin B12 might (and might not) help our hair.

Finally, we’ll outline some potential best-practices for those who want to supplement with vitamin B12 for hair growth. After all, too little (and too much) of this vitamin may be counterproductive to both our hair and overall health.

What is vitamin B12?

Vitamin B12 is a singular vitamin apart of the greater B complex family. Like many B vitamins, vitamin B12 acts as an enzymatic cofactor for essential functions of the body (1). Specifically, vitamin B12 helps us metabolize food, produce red blood cells, and “methylate” DNA (more on this later). It also plays a protective role in cardiovascular health, as it helps to reduce excess amounts of a protein called homocysteine – which, at high levels, is inflammatory.

Vitamin B12 Supplement Mockup

Given its importance in so many bodily functions, it’s natural to wonder: does vitamin B12 also help fight hair loss? After all, it seems to be a staple ingredient in most hair health nutritional supplements. So, what does the evidence show?

The case for a vitamin B12-hair loss connection

From a scientific perspective, vitamin B12 might support hair growth in many ways.

1. Vitamin B12 help support the production of DNA – which is necessary to maintain the rapid cell division that drives hair growth (2). Without cell division, not only can hair not grow… but human life cannot sustain itself, either. In this respect, technically anything that supports human survival – even water – supports hair growth.
2. Vitamin B12 helps us produce hemoglobin – a molecule inside our red blood cells that carries oxygen and iron into our tissues (3). When someone has low hemoglobin, they often have an iron deficiency (i.e., anemia). Interestingly, anemia is highly correlated with hair loss – particularly in women ages 14-40 – and vitamin B12 supplementation can help improve hemoglobin product and thereby iron levels for those who are deficient.

But there’s also another reason that vitamin B12 might support hair growth – and it happens to do with one of the biggest buzzwords surrounding this vitamin: methylation.

In the simplest terms, methylation is a way in which our bodies can “turn on” or “turn off” certain genes. In other words, methylation helps change our gene expression – and thereby influences our ability to prevent cancer, reduce inflammation, and everything in between.

Here are just a few roles that methylation – and our methylation cycle – regulates inside our bodies:

• Production of methionine and cysteine. These are two sulfur-based amino acids that play integral roles in muscle building, inflammation regulation, and antioxidant production.
• Glutathione production. Sulfur amino acids are a major precursor for glutathione, the body’s master antioxidant.
• Homocysteine reduction. High levels of homocysteine in the blood are linked to a variety of inflammatory diseases.
• Production of SAMe. This protein is believed to support mental health, among many other things (4).

So, how does methylation relate to B12 and hair loss?

In one study on rabbits, researchers found methionine to be a promoter of hair growth. The mechanism behind this? An increase in the activity of the Wnt/β-catenin signaling pathway (5).

The Wnt/β-catenin pathway is important to this discussion for a few reasons:

1. This pathway helps promote the creation of stem cells, which are required for hair growth and hair follicle function (6).
2. In androgenic alopecia (AGA) – the most common form of hair loss in adult men – male hormones interfere with Wnt/β-catenin signaling. Specifically, this signaling pathway is dampened, also known as downregulated. As a result, hair follicle stem cell activity is impaired, which prevents proper hair cycling. This shortens the growth stage of a hair follicle, causing it to prematurely shed. Over time, this hinders hair growth and may even accelerate hair follicle miniaturization – a defining hallmark of male and female pattern hair loss (7).

Here’s where vitamin B12 might come into play:

Vitamin B-12 is a cofactor in the methylation cycle, meaning that it helps to activate methylation. Interestingly, vitamin B-12 deficiencies are believed to be a major driver of a dysfunctional methylation cycle – as evidenced by an association between homocysteine levels and vitamin B-12 deficiency (8). This suggests that the methylation cycle is “backed up”, preventing homocysteine from being converted to cysteine and methionine.

Thus, B-12 deficiency may impair methionine synthesis from the methylation cycle. Because we know that methionine contributes to Wnt/β-catenin signaling, it’s possible that a reduction in methionine may lead to reduced Wnt/β-catenin activity. And therefore, it’s possible that a vitamin B12 deficiency in scalp tissues might play a role for people dealing with androgenic alopecia.

Summary (so far): how vitamin B12 might help fight hair loss

There are a variety of ways that vitamin B12 might be connected to hair loss in humans:

• Vitamin B12 helps support DNA synthesis. Without DNA synthesis, we would die. We can’t grow much hair if we’re dead.
• Vitamin B12 helps normalize hemoglobin production (and thereby iron levels). For females with both hair loss and an iron deficiency, vitamin B12 might be a great way to improve iron status and encourage hair growth.
• Vitamin B12 helps support methylation. This might have ramifications for one of the world’s most common hair loss disorders – male pattern hair loss (AGA. In AGA-affected hair follicles, the Wnt / β-catenin signaling pathway is dampened, which leads to shorter-growing hair, premature hair shedding, and potentially even hair follicle miniaturization. If this happens to be the direct result of a deficit in localized methylation in scalp tissues, then vitamin B12 might help improve methylation and thereby improve Wnt / β-catenin signaling, which would allow for hairs to grow longer, shed less prematurely, and (hopefully) not miniaturize as quickly.

But it’s important to stress: these suspected mechanism are all hypothetical. Yes, vitamin B12 is connected to each mechanism. Yes, these mechanisms are linked to hair loss (and hair growth). But there’s a difference between association and causation. And this difference, unfortunately, is consistently forgotten by companies trying to sell you B12 supplements. Thus, to prove a strong association or causation, the real questions we should be asking are:

1. Are vitamin B12 deficiencies (in skin tissues or throughout the body) observed more frequently in people who are balding?
2. Does vitamin B12 – through supplementation or topical application – actually improve hair loss outcomes?

In answering these questions, we can actually discern whether or not it makes sense for most people to spend money on vitamin B12 supplements to try and regrow their hair.

And as you can guess, these questions happen to lead us to our next section: the case against a vitamin B12-hair loss connection.

The case against a vitamin B12-hair loss connection

While there is hypothetical evidence linking vitamin B12 to hair loss and hair growth, this argument begins falls apart when we zoom out and start looking at the broader evidence.

Specifically, we’re going to talk about the following:

1. Misconceptions about methylation, B12, Wnt/β-catenin pathways, and hair loss
2. Vitamin B12 levels of hair loss patients
3. Observations in birth control-induced vitamin B12 deficiencies, and what this does (or doesn’t do) to hair

Methylation misconceptions

Earlier we discussed how, in balding hair follicles, a deficiency in the methylation cycle might interfere with Wnt/β-catenin signaling pathways, which might accelerate hair loss. We argued that because vitamin B12 supports methylation, this vitamin might also help reverse this methylation deficiency, and thereby help fight hair loss from androgenic alopecia.

But it’s important to note: vitamin B12 is just one (of many) vitamins and nutrients that support methylation. For instance, many other B-vitamins also support methylation, and these B-vitamins are found in abundance in foods like beef, eggs, and poultry.

This means that even if you do have a vitamin B12 deficiency, your body will likely be able to compensate for this – at least from a methylation perspective – via your dietary choices. Therefore, in balding hair follicles, even if Wnt / β-catenin downregulation were exclusively due to a methylation issue (it isn’t), your body would still have many “fallback” vitamins to address that methylation issue. So, in androgenic alopecia, changes to a hair follicle’s gene expression cannot be significantly attributed to a vitamin B12 deficiency.

Therefore, it also shouldn’t be surprising to find out that there aren’t any differences in vitamin B12 levels between those with and without hair loss.

Looking at B12 levels in the blood of hair loss patients

When we zoom out beyond the actual hair follicle and look at studies on people with common hair loss disorders like AGA, telogen effluvium (TE), or alopecia areata (AA) – the data are consistently clear: there is no difference in blood measurements of vitamin B12 between people with and without hair loss (9). In other words, people who are losing their hair and who have full heads of hair appear to have the same vitamin B12 levels.

Even more compelling, recent literature reviews have found no evidence to support the use of vitamin B12 for hair loss of any type (9). That means that not only are vitamin B12 levels the same across those with and without hair loss, but that for those with hair loss, vitamin B12 supplementation generally doesn’t improve hair loss outcomes.

What about women with hair loss due to an iron deficiency? Doesn’t vitamin B12 help improve iron stores, and have some therapeutic benefit here?

Yes and no.

Earlier, we argued a connection between hemoblogin, iron, vitamin B12, and hair loss. As a refresher, hemoglobin is a molecule found in red blood cells. Hemoglobin carries oxygen and iron, and in general, when someone has low hemogloblin levels, they also have low iron (10). Low iron levels are often found in women ages 14-40 with hair loss. Vitamin B12 is a key cofactor in hemoglobin formulation. Therefore, you might be able boost hemoglobin production with vitamin B12, and therefore potentially normalize low iron levels. If someone is dealing with hair loss as a direct result of low iron levels, then vitamin B12 supplementation might help to normalize these levels and maybe regrow some hair.

So, in a situation where someone’s hair loss is due to poor iron status, and their poor iron status is a direct result of low vitamin B12, then it absolutely makes sense to supplement with vitamin B12. In doing so, you’d improve hemoglobin production, oxygen and iron transport, and (very likely) hair loss outcomes. This is why a lot of popular hair loss supplements – like Nutrafol – contain B12.

At the same time, a vitamin B12 deficiency is only one possible contributor toward an iron deficiency. A more likely contributor? A deficiency in iron itself (11). So, while vitamin B12 is probably therapeutically useful in some circumstances of iron deficiency-related hair loss, it’s not the only reason – or even the biggest reason – for why the iron deficiency arises.

Therefore, B12 is likely useful for a much smaller percentage of women than advertisements for these hair health supplements might lead you to believe.

Observations in birth control-induced B12 deficiency

This argument is further strengthened by another observation researchers have made: women with vitamin B12 deficiencies caused by hormonal birth control don’t experience hair loss or adverse changes to hair growth (9). As such, even when a deficiency is present, it doesn’t seem to negatively impact hair growth. In fact, many women on hormonal contraceptives report the opposite effect – hair regrowth – which is why some contraceptives are also used off-label as a hair loss treatment.

The good news? Vitamin B12 might help reverse premature hair graying

In regard to hair health, there is one way that vitamin B12 might positively impact hair health outcomes. It might help to prevent, or even reverse, premature graying.

To be clear, the majority of research doesn’t indicate B12 deficiency is a cause of hair loss. But, there are several reports supporting an association between inadequate B12 levels and premature hair graying, which is grey hair that onsets before the ages of 20-30 (depending on the demographic) (12).

For instance, one small study demonstrated that individuals with premature hair graying had lower vitamin B12, folate, and biotin levels than control subjects without premature gray hair (13). Additionally, some studies report a higher incidence of premature graying in pernicious anemia, a blood condition sometimes caused by B12 deficiency (14).

There are also three case reports of patients reversing their premature gray hair with B12 supplementation (15-17). Needless to say, there seems to be evidence of both an association of low B12 and early greying, and a reversal of early greying following B12 supplementation.

The association between B12 deficiency and premature graying isn’t fully established, and there are absolutely other factors that can lead to premature hair graying. Moreover, B12 supplementation is really only relevant to reversing graying hair in the context of B12 deficiency.

That being said, a vitamin B12 deficiency may be worth investigating for anyone experiencing premature hair graying – regardless of whether you’re losing your hair.

The verdict: in most situation, vitamin B12 likely has no effect on hair loss (and hair regrowth), but vitamin B12 might reverse premature hair graying in the presence of B12 deficiency

Although hypothetical evidence suggests an absence of B12 activity could negatively impact hair growth, in vivo human studies indicate that either (1) there is no relationship between vitamin B12 deficiency and hair loss and/or (2) there is an overriding factor (like methionine provision outside of the methylation cycle) that prevents B12 deficiency from causing hair loss.

The exception to this is if someone has iron deficiency-related hair loss, and if their iron deficiency is exclusively the result of poor hemoglobin production due to a vitamin B12 deficiency. In this case, vitamin B12 supplementation can address the deficiency, improve hemoglobin production, and thereby drastically improve iron transport (and, ultimately, hair growth). But it goes without mentioning that this is a very specific scenario that is not faced by the majority of hair loss sufferers in the developed world.

In any case, it’s clear that supplementing with B12 is probably not the best solution for improving hair growth – at least as a standalone therapy.

That being said, it’s important to note that having adequate B12 is essential for optimal health. Even if it doesn’t cause hair loss, B12 deficiency can still lead to anxiety, fatigue, neuropathy, and cardiovascular issues, among other health issues. Moreover, B12 deficiency appears to be one potential cause of premature hair graying.

As such, even if it doesn’t improve hair loss, some may still find it necessary to supplement with vitamin B12. So, in these cases, what’s the best approach for supplementation?

Things to keep in mind when supplementing with vitamin B12

Vitamin B12 supplements are available in three forms: cyanocobalamin, methylcobalamin, and adenosylcobalamin. Methyl- and adenosylcobalamin are naturally-occurring forms of B12 whereas cyanocobalamin is synthetic.

Though synthetic is not always subpar to naturally-occurring forms of B12, in this case, supplementing with methyl- and adenosylcobalamin B12s is much more efficient. The reason for this is they are already in their active forms, ready to be used by the body. Cyanocobalamin, on the other hand, requires enzymatic processing before it can be utilized. On top of this, cells don’t seem to retain cyanocobalamin as well as some of the other forms (18).

Additionally, some researchers have raised concerns with long term cyanocobalamin supplementation, due to the cyanide present in the compound (18). Even though these concerns aren’t yet substantiated, an abundance of caution may be warranted here.

The bottom line? If your diet isn’t providing you with enough vitamin B12 and you choose to supplement, consider opting for a B-complex or multivitamin formulated with methyl- or adenosylcobalamin.

Summary

Vitamin B12 deficiency isn’t likely to be a cause for hair loss. As such, claims that supplementing with B12 will improve hair growth are largely unfounded. This is despite some pretty compelling theoretical evidence – like B12’s role in hemoglobin formation, nucleic acid synthesis, and the methylation cycle that produces growth-supporting methionine.

It just goes to show how important it is that we don’t rely on studies of isolated nutrients in cell cultures. Moreover, we shouldn’t have high hopes for products marketed on these premises when it comes to regrowing our hair.

That being said, vitamin B12 deficiency can still cause real problems and, in some cases, may be an underlying factor in premature hair graying. So, for those who are dealing with early-onset gray hair, it may be worth checking your B12 levels. And if you are deficient? Restoring your B12 levels may just reverse the condition.

So, if supplementing is warranted in your case, opt for a methyl- or adenosylcobalamin-containing supplement over one containing cyanocobalamin. They’re more bioavailable and may be safer in the long-term.

But, for the overwhelming majority? You’re likely to get all the vitamin B12 you need from food — more than enough to rule it out as a plausible factor in hair loss.

Have any questions about vitamin B12? Leave them below.

Alopecia areata is an autoimmune form of hair loss that affects 2% of people worldwide. If you’re dealing with alopecia areata, the burden of hair loss often feels overwhelming – as the condition can progress rapidly, inexplicably, and without regard.

Fortunately, alopecia areata is treatable. In many cases, it’s also reversible. The first step toward making progress? Understanding alopecia areata, its myriad triggers, and how these factors relate to your unique hair loss situation.

In this article, we’ll uncover the characteristics of alopecia areata: its clinical presentations, histological features, and more. We’ll also dive into alopecia areata’s causes: what we know, what we don’t, and what this type of hair loss can tell us about our health.

Finally, we’ll outline treatments for alopecia areata (both conventional and natural): the research supporting them, the expectations for regrowth, and who might be the best candidates for each intervention.

What is alopecia areata?

Alopecia areata (AA) is a form of hair loss driven by autoimmunity. To put it simply, alopecia areata occurs when our bodies mistakenly recognize our hair follicles as foreign invaders, and then begin to attack our hair follicles. This leads to the dysfunction of hair follicle stem cells, and eventually, hair loss.

What does alopecia areata look like?

You might know alopecia areata (AA) from its “patchy” presentation, whereby slick-bald patches begin to form in a non-uniform fashion. But AA can also vary in appearance – and even mask the look of many other common hair loss disorders.

Types of alopecia areata
Alopecia areata focalis or “patchy” alopecia areata	Hair loss in patches, can extend beyond just the scalp. The most common form of alopecia areata. It may or may not progress into alopecia totalis or alopecia universalis.
Alopecia areata totalis	Loss of all hair on the scalp including eyelashes and eyebrows.
Alopecia areata universalis	Hair loss of the scalp, eyelashes, eyebrows, and whole body, including all body hair.
Ophiasis or alopecia areata marginata	Hair loss around the circumference of the head in a band-like fashion. It is most commonly seen behind the ears and the nape of the neck, but can occur in the frontal hairline and extend throughout the scalp in severe cases, as well.
Ophiasis inversus	Hair loss that begins in the center of the scalp and progresses into the surrounding regions.
Alopecia areata incognita	Diffuse hair loss whereby no specific bald “patches”, normally characteristic of alopecia areata, can be distinguished.

What’s the histology of alopecia areata?

Histology is a term used to describe a close-up view of a tissue’s structure. In the world of hair loss, histology refers to the microscopic view of a hair follicle (i.e., what a hair follicle looks like when biopsied).

When doctors are uncertain about someone’s hair loss diagnosis, they’ll often take a biopsy of their patient’s scalp so that they can get a look of the histological features of the affected hair follicles. Then, they’ll compare what they see against the histological hallmarks of certain hair loss disorders.

It might sound invasive, but these scalp biopsies are perhaps the most effective way for dermatologists to definitively diagnose someone’s hair loss. And when it comes to alopecia areata, this type of hair loss has a lot of interesting features:

• Inflammation. Specifically, the infiltration of lymphocytes near hair follicle stem cell bulges. Lymphocytes are immune cells; the bodies uses them as part of an inflammatory response. Where there are high lymphocytes, there are usually high amounts of inflammation. One study found that 84% of alopecia areata subjects presented with this kind of inflammation.
• Dysfunctional hair follicle stem cell bulges. Hair follicle stem cells contain the blueprints to make new hair follicles. When too many lymphocytes collect near these stem cells, they generate inflammation, and that inflammation interferes with the ability for these stem cells to function. This leads to stem cell dysfunction and an inability to form new hair.
• Hair follicle miniaturization. This is a decrease in hair strand diameter, which leads to thinner-looking hair. One study observed that 90% of alopecia areata subjects had hair follicle miniaturization. Conversely, this study only found miniaturization in 25% of subjects. This study found that the presence of miniaturization is likely dependent on the nature of the hair loss – for example, early stages of AA likely do not present with miniaturization. It is most commonly often found in recurrent and chronic forms of AA.
• Increased number of catagen hairs. This study found that 93% of patients presented with an abnormally high number of hair follicles in the catagen phase – the phase in the hair cycle whereby nutrient supply is cut off and the hair prepares to shed. In healthy scalps, only 1% of hair follicles are typically in catagen. With AA, that percent can skyrocket.

Isn’t inflammation & hair follicle miniaturization part of androgenic alopecia (AGA)?

Yes.

Pattern hair loss, also known as androgenic alopecia (AGA), is also often defined by the presence of inflammation, hair follicle miniaturization, and even an increased number of catagen and telogen hairs. This begs the question: how can we distinguish between AGA and alopecia areata… especially in cases where alopecia areata is diffuse?

Well, there are some additional factors that can help us identify if we’re dealing with alopecia areata (AA) or androgenic alopecia (AGA).

What makes alopecia areata (AA) unique from androgenic alopecia (AGA)?

1. The patterning of AA. In most AA cases, hair loss begins in a “patchy” fashion — a patterning that is exclusive to AA. In contrast, AGA occurs in a very different, yet still distinct manner. For men, it’s temple recession and crown thinning. For women, it’s most often a widening of the part while their hairline stays intact (also known as a “Christmas tree” pattern).
2. Exclamation-point hairs in AA. Exclamation point hairs, pictured below, are a phenomenon only observed in AA. These hairs remain thick along the shaft but are noticeably thinner towards the opening of the follicle, creating an appearance akin to that of an exclamation mark ( ! ). This is only a defining factor if hair is still present.

   1. Exclamation mark (!) hair
      

3. Pigment casts in AA. Melanin is a substance produced by cells to create pigment for our skin and hair. Interestingly, in cases of AA, there are often “clumps” of melanin deposits throughout the follicular unit. This can appear like a small, dark tattoo where there should be a hair follicle. The incidence of pigment casts varies from study to study from 44% to 72%. Having said that, pigment casts by themselves aren’t a good indicator of AA – mostly because they’re often observed at similar rates in other hair loss disorders like trichotillomania (i.e., a “hair-pulling disorder”).

What causes alopecia areata?

To reiterate from earlier, inflammation seems to initiate of AA. The process looks like this:

1. Inflammatory cells infiltrate the area surrounding a hair follicle stem cell bulge.
2. This inflammation disrupts stem cell functionality, leading to stem cell dysfunction.
3. These dysfunctional stem cells stop producing normal-looking hair follicles.

This leads to:

• Rapid hair follicle miniaturization (i.e., exclamation hairs).
• A loss of visible hair (i.e., slick-bald patches in alopecia areata focalis).
• Weaker, brittler hair that breaks off soon after growing out of the skin surface.

This begs the question… when it comes alopecia areata, what causes the inflammation that kickstarts the whole process?

What causes the inflammation in alopecia areata?

While the exact origin of inflammation isn’t known, researchers have a good idea of three contributing factors: genetics, environmental triggers, and loss of immune privilege in the follicle.

And though we don’t know the exact nature of these contributing factors, researchers have begun to uncover some of the details:

• Genetics. Studies have shown that AA is common among family members, affirming the role of a genetic component in certain cases. Specific genes affected include those that code for immune cell receptors, cell death coordination, immune-regulating cells, other proteins that regulate cellular communication.
• Environmental factors. Much like genetics, environmental elements faced by AA-affected families might also explain why this condition tends to appear multiple times within the same family. These environmental factors include
  • Stress
  • Infections
  • Hormone fluctuations
  • Dysbiosis of the gut flora
  • Oxidative stress
  • Soy consumption (implicated in animal studies, though not yet confirmed in human studies)
  • Nutrient deficiencies (specifically, vitamin A and/or vitamin D deficiency.
• Loss of immune privilege. Under normal circumstances, a hair follicle produces its own “shield” from our own immune system. This shield is comprised of many immune-suppressing molecules. This is known as immune privilege, and it’s what make hair follicles incredibly unique mini-organs. However, in AA, researchers believe this immune privilege collapses – preventing the hair follicle from protecting itself against a damaging attack by the immune system. This would lead to inflammation and, thereby, the destruction of the hair follicle stem cell bulge. How this occurs is unknown, but researchers believe it is a result of proteins secreted by skin cells that the body forms an “antibody” to, leading to an immune attack.

What are the available treatments?

Currently, there are a variety of drug and non-drug treatments for AA. But before we reveal them, there are two things worth mentioning:

1. Because we don’t fully understand why AA occurs, the most well-studied treatments primarily focus on suppressing the signals that lead to AA (as opposed to treating its root cause). More recent research has explored treatments that try to target some of these potential root causes. These studies show promise, but they’re also a little “out there” in terms of peoples’ comfortabilities. So, as you read on, keep this in mind.
2. When it comes to reversing alopecia areata, 34-50% of cases resolve spontaneously. This makes it hard to know which treatments work, and which treatments just happened to coincide with spontaneous reversals. This is why control groups are so important in AA studies. Moreover, the likelihood of spontaneous reversal depends highly on the progression of the disease: as AA progresses, the likelihood of spontaneous resolution declines.

Regardless of these factors, it seems like treating AA in earlier stages leads to better outcomes and decreases the risk of future treatment resistance. So, if you’re facing AA right now, it’s best not to place your bets on a spontaneous reversal; rather, hedge those bets with the treatment options at your disposal (or at least the ones you’re comfortable trying).

The following sections detail many conventional and alternative treatments: the evidence, best practices, mechanisms of action, and more.

Drug-based treatments

Topical, intralesional, and systemic steroids (first line of treatment)

• Best candidates: Patchy AA may be controlled with topical or intralesional steroids. More severe or resistant cases (alopecia totalis, alopecia universalis, ophiasis) may require systemic steroid treatment or combination therapy (steroids + other treatments).
• Mechanisms of action: Reduction of inflammation.
• Dosages: For topical steroids, concentrations vary from 0.05% to 0.25%; for intralesional steroids, most commonly-used agent is triamcinolone acetonide, at concentrations of 2.5 mg/mL to 10 mg/mL; for systemic steroids, varying doses given as pulse doses, a.k.a large bolus doses for a specific period of time, administered in intervals.
• Outcomes: Results vary between methods of administration. Topical steroids are best suited to earlier stages of AA, with about 57% of these patients demonstrating complete regrowth. Intralesional steroids have a slight advantage over topicals, with 63% of patients achieving complete growth in one study. Systemic steroid treatment is primarily relegated to resistant cases.
• Problems: With topical and intralesional treatment, the main side effect is cutaneous atrophy or thinning of the skin. Systemic steroids come with a higher risk of side effects, and these risks may outweigh the benefits of hair growth. The relapse rate after steroid treatment ranges between 33% and 75%.

Janus kinase (JAK) inhibitors (oral and topical)

• Best candidates: Men, women, and children with patchy AA, alopecia universalis, alopecia totalis, according to preliminary evidence.
• Mechanisms of action: Blocks inflammatory signaling.
• Dosages: 5mg twice per day.
• Outcomes: Efficacy is similar in patchy alopecia areata, alopecia universalis, and alopecia totalis as well as in both men vs. women and adults vs. children. Oral administration is more likely to produce a good response when compared to the use of topical applications. Studies show initial hair growth occurs as soon as 2 months, with full regrowth occurring in an average of 6 months.
• Problems: Evidence is limited and primarily in the form of case reports. As such, though JAK inhibitors show promise, we don’t know a lot about the safety or efficacy of these medications in AA, yet. Drugs in this class have been linked to an increased risk of upper respiratory issues, latent virus reactivation, and cancer. The exact risk of these adverse effects in the treatment of AA is unknown, however, upper respiratory infection was the most common among available case studies. Like other therapies in AA, there is a high rate of relapse after cessation of the drug.

Immunotherapy (dinitrochlorobenzene, squaric acid dibutylester and diphenylcyclopropenone, with diphenylcyclopropenone)

• Best candidates: Mild to moderate patchy alopecia areata.
• Mechanisms of action: Immunogenic compound “distracts” the immune system with a more stimulating antigen than the self-antigen the mediates the autoimmune reaction.
• Dosages: Concentration sufficient enough to induce an allergic response.
• Outcomes: Response rates as reported in the literature range widely, from about 9% to 87%. About 20% to 30% of patients are able to achieve significant hair growth, such that they are able to manage their hair loss without a wig. This specific therapy may require longer treatment times, as evidenced by over a two-fold increase in response rate at 32 months versus 6 months. So, ask your doctor about whether a longer treatment period might be right for you. In over 30 years of use, long-term side effects have not been reported with immunotherapy, however, some side effects can occur during therapy. The most common side effect is cervical and occipital lymphadenopathy and severe dermatitis, however, these only last for the duration of the therapy. Moreover, dermatitis can be avoided by using the proper concentration of the antigenic compounds. Vitiligo and itching have also been reported but are considered rare. Overall, the treatment appears to be well-tolerated and effective.
• Problems: As with most treatments, relapse rates are high at around 62%. Response rates are somewhat low when administered for the same treatment periods as other treatments. In other words, immunotherapy takes longer to work than other treatments.

Minoxidil

• Best candidates: Mild patchy AA, AA patients tapering off of steroid therapy
• Mechanisms of action: Not fully known, but is believed to stimulate the “anagen” growth phase of the hair cycle, thereby promoting regrowth of lost hairs.
• Dosages: 2% or 5% minoxidil, two to three times daily.
• Outcomes: In one study, 85% of patients using 5% minoxidil alone experienced regrowth, however, this regrowth wasn’t cosmetically significant. Another study demonstrated that the application of 2% minoxidil, when applied three times daily, helped retain hair regrowth after tapering off of steroid treatment.
• Problems: Minoxidil doesn’t seem to be that effective outside of post-steroid hair retention.

Methotrexate

• Best candidates: Moderate to severe AA, including universalis, diffuse, and totalis phenotypes.
• Mechanisms of action: Suppression of the immune system.
• Dosage: 10-25mg per week + folate/folic acid supplements (methotrexate depletes folic acid).
• Outcomes: One study reported that 44.4% of subjects taking methotrexate were able to regain 50% or more of their hair as observed in a follow-up period ranging from 3 to 51 months. The best responders were males, those with multifocal patchy AA (followed by totalis, then universalis, and, lastly, diffuse), and those who used a cumulative dose of 1,000 to 1,500mg. When corticosteroids were used alongside methotrexate, the number of patients regrowing at least 50% of their hair increased to 77.3%.
• Problems: Methotrexate isn’t well-studied for AA — the evidence is primarily made up of case studies. 3-24% of patients can expect to experience side effects like mild to moderate leukopenia, thrombocytopenia, and megaloblastic anemia. There is also the risk of liver fibrosis, with an incidence ranging from 7% to 71.8%. Such a wide range makes the true risk hard to quantify. Myelosuppression is also a dangerous side effect and its risk associated with methotrexate use is unpredictable. Relapse rates vary from 33% to 80%, with some studies suggesting the rate is associated with how much hair is gained during treatment — more hair regrowth during treatment is associated with a lower risk of relapse after treatment.

Non-drug based treatments

Fecal microbiota transplant (FMT)

Fecal microbiota transplant (FMT) is a procedure whereby gut bacteria are isolated from a donor’s feces, purified, and then transplanted into an FMT candidate. This is the only procedure in which bacterial strains that have been lost from the gut can be reinoculated.

Currently, the procedure is elective in Europe (anyone can elect to have it performed). But in the U.S., it’s only available for chronic C. difficile infections. In the U.K., Taymount Clinic is one of the most popular worldwide-serving clinics for elective FMT.

• Best candidates: Evidence is limited but FMT has been used to treat patchy AA and alopecia universalis. May also be effective in treatment-resistant cases.
• Mechanisms of action: Unknown, but probably a normalization of the gut flora, leading to reduced autoimmune activity.
• Dosage: N/A; donor transplant is performed in one procedure, although people often elect for multiple procedures (depending on the delivery method).
• Outcomes: There are currently three case studies (studies here and here) investigating the efficacy of FMT in AA: two in alopecia universalis and one in patchy AA. Of the 3 case studies, all patients showed marked improvement following FMT — with two cases of almost full regrowth (one in universalis alopecia and one in patchy AA) and one case of partial regrowth. In all cases, this hair regrowth was sustained for at least 1.5 to 3 years. Considering the relapse of AA for most treatments is high, this sustained regrowth is promising. However, whether or not this regrowth was sustained beyond the follow-up period is unknown.
• Problems: FMT is still considered an investigative treatment in the U.S. and is, therefore, not elective for individuals with AA, unless a patient is also dealing with chronic C. difficile infection. As such, US residents wanting to explore the treatment must travel for the procedure and pay for it out-of-pocket — these costs can rack up (but may be worth it in the long run).

FMT before & after photos

Case #1: (A) 1 month, (B) 4 months, (C) 1.5 years after FMT in patchy AA

Case #2: (A) The patient’s scalp when his AA first began (B) a few months, (C) 1.5 years after FMT in alopecia universalis

Case #3: The beginning of hair regrowth after FMT in a case of long-standing alopecia universalis

Essential oils

• Best candidates: Evidence is limited, however, efficacy has been demonstrated for general AA in one study. In this specific study, the authors did not specify which kind of AA patients were dealing with.
• Mechanisms of action: Unknown, but probably a reduction in inflammation.
• Dosage: 2 drops thyme essential oil (EO), 3 drops lavender EO, 3 drops rosemary EO, 2 drops cedarwood EO diluted in 3mL jojoba oil and 20mL grapeseed oil.
• Outcomes: In this study, 54% of AA patients in the active group experienced hair regrowth over 7 months while 46% experienced no change (however, hair loss also did not get worse). A majority of these patients achieved hair regrowth in the 10-30% range, followed by 81-100%. In contrast, 78% of the placebo group did not improve, suggesting the essential oil mixture did, indeed, have an effect. It’s likely that the remaining 22% were experiencing spontaneous remission. Neither group experienced adverse side effects.
• Problems: It’s not clear just how many patients may benefit from EO application given that spontaneous resolution is a common occurrence. We see evidence of this in the placebo group, which may be a confounding factor in the measurement of treatment efficacy (since we don’t know how many in the active group would have resolved without intervention). Taking this into account, the response rate, when compared to other treatments for AA, is relatively low. Another issue is the fact that the study did not have a designated follow-up period to measure the rate of relapse. Therefore, we can’t be sure of just how effective this treatment is in the long run. Moreover, the treatment period was quite long in comparison to what is normally employed with other therapies. Given that AA can become more treatment-resistant as time goes on, using topical EOs may delay appropriate treatment and, as a result, require more aggressive therapies in the future.

Onion juice

• Best candidates: Men and women with patchy AA.
• Mechanisms of action: Unknown, but researchers believe it could work similarly to immunotherapy.
• Dosage: Application sufficient to cover the affected area(s) twice daily.
• Outcomes: This study found that patients with patchy AA were able to see hair regrowth as early as 2 weeks into the study period. Full hair regrowth was seen in 86.9% of patients after 8 weeks. Contrastingly, hair regrowth was only observed in 13% of the control group, making the findings of this study statistically significant.
• Problems: This study, unfortunately, had no follow-up period. As such, we don’t know how many patients experienced a relapse after cessation of treatment. Moreover, the smell of onion juice may make this treatment hard to adhere to long-term.

Garlic gel

• Best candidates: Men and women with mild patchy AA.
• Mechanisms of action: Unknown, but researchers believe it could work similarly to immunotherapy.
• Dosage: 5% garlic gel with 0.1% betamethasone valerate gel, twice daily.
• Outcomes: This study found that garlic was able to enhance the hair growth-promoting effects of a corticosteroid, betamethasone valerate. After 3 months, the active group was able to achieve a significant reduction of hair loss patches — more so than the corticosteroid topical alone.
• Problems: Like the onion juice study, this study (1) did not measure the rate of relapse after cessation of therapy and (2) fails to account for the smell, which may make the treatment difficult to adhere to in real-world settings.

Capsaicin

• Best candidates: Patients with patchy AA and, possibly, alopecia totalis.
• Mechanisms of action: Unknown, but researchers suspect neuroimmunological modulation in the hair follicle.
• Dosage: 0.075% capsaicin topical applied daily.
• Outcomes: Studies employing the use of capsaicin have show varying results. Some studies report the regrowth of vellus hairs, but no appreciable regrowth sufficient to justify its use over other treatments, while others report hair growth in just 3 weeks.
• Problems: Evidence suggests capsaicin may promote some degree of regrowth, but not enough to justify its use over other treatments — especially considering that AA becomes increasingly treatment-resistant over time. Thus, capsaicin use may delay appropriate treatment and, thus, increase the risk of refractory AA in the long-run.

Vitamin D repletion

• Best candidates: Patients with patchy AA and vitamin D deficiency and/or genetically reduced vitamin D receptor expression.
• Mechanisms of action: Likely a modulation of autoimmune activity in the follicle, due to vitamin D’s widespread effects on balancing the immune system.
• Dosage: For oral vitamin D use, the dosage will vary depending on the severity of vitamin D deficiency and whether your practitioner decides to opt for weekly bolus or daily doses. For topical vitamin D therapy, topical applications range from 0.005% calcipotriol twice daily to 50 micrograms/mL calcipotriol once daily.
• Outcomes: Evidence from meta-analyses show that AA patients are more likely to be vitamin D deficient than healthy controls. This would suggest that vitamin D could be beneficial to AA patients, however, no studies have been conducted to assess clinical benefit. The topical application of vitamin D-like, conversely, has been investigated as a treatment avenue. These studies show that twice daily application of various concentrations results that vary from 50% regrowth all the way to clinical remission (full hair regrowth). One study found that efficacy was associated with lower vitamin D levels at the beginning of the study, suggesting that lower vitamin D levels may be a marker of a good candidate. Additionally, one case report demonstrated full clinical remission in a patient with AA and reduced vitamin D receptor expression. Thus, AA patients with low vitamin D levels or reduced vitamin D receptor expression may have the best response to treatment. Studies also show minimal risk of adverse side effects.
• Problems: Studies do not currently show benefit in more severe cases of AA, like alopecia totalis or alopecia universalis. There is limited evidence investigating the therapeutic potential of oral supplements.

Zinc

• Best candidates: Patients with mild AA and zinc deficiency.
• Mechanisms of action: Unknown, but could be attributed to antioxidant regulation and anti-inflammatory activity.
• Dosage: Dosage depends on the severity of the deficiency, however, doses between 50 and 220mg have been used in the literature.
• Outcomes: Studies suggest AA patients have lower zinc levels compared to healthy controls. Interestingly, evidence also suggests a correlation between zinc levels and treatment resistance, meaning zinc deficiency may have an emerging role in refractory AA. However, some studies have failed to find a relationship between zinc and AA. Moreover, some studies show no benefit with zinc supplementation while others suggest zinc therapy may be beneficial in the context of mild AA with zinc levels below 70 μg/dL. Overall, the role of zinc therapy in AA is unclear other than zinc deficiency is more common among AA patients. Nonetheless, zinc repletion may confer health benefits in the presence of deficiency, even if clinical regrowth is not achieved.
• Problems: Research is mixed, with some studies suggesting benefit and others suggest a net zero effect. Thus, there is no conclusive evidence to support the use of zinc in AA.

Azelaic acid

• Best candidates: Patients with patchy AA.
• Mechanisms of action: Unknown, but preliminary evidence suggests it may act similarly to that of immunotherapy.
• Dosage: 20% azelaic acid topical applied twice daily.
• Outcomes: Evidence supporting the use of azelaic acid in patients with AA is lacking. However, one pilot study demonstrates efficacy on par with anthralin, a medication used to treat psoriasis (another autoimmune disease that affects the skin). Just over half of the patients tested achieved complete regrowth with both treatments with no report of adverse events.
• Problems: Research is limited and, as such, the true efficacy of azelaic acid is not known. Moreover, the aforementioned study did not employ a follow-up period, which is necessary to estimate the rate of relapse.

Platelet-rich plasma (PRP)

• Best candidates: Patients with ophiasis-pattern AA resistant to steroid treatment or AA patients who develop side effects with steroid treatment.
• Mechanisms of action: Unknown, possibly immunomodulatory effects.
• Dosage: 9 mL injection.
• Outcomes: In one case study of steroid-resistant ophiasis AA, a form of AA which is generally hard to treat, the patient was able to achieve regrowth by month 1 with significant regrowth by month 3. The patient reported no side effects. Another study demonstrated the superiority of PRP over steroid injections for patchy AA.
• Problems: Unfortunately, there is limited evidence available. The rate of relapse is unknown. The procedure is also costly.

Case study: ophiasis-type AA before and 3 months after PRP treatment.

Brotzu Lotion

Brotzu lotion is a topical formulated by Dr. Brotzu. It contains three main compounds: dihomo-gamma-linoleic acid, S-Equol, and propionyl-L-carnitine — ingredients designed to target inflammation and decreased blood flow in follicles.

There is currently no clinical evidence to support the efficacy of Brotzu lotion in AA. Nonetheless, some initial case studies do show promise. Take, for example, these two before-and-afters:

Brotzu Lotion: a child with alopecia universalis

And here’s a case of near-complete recovery of patchy AA in just 16 months from Dr. Brotzu’s presentation at this conference — start at 10:30):

Brotzu Lotion: alopecia areata recovery

While these are the only case studies we have pictures of, Dr. Brotzu’s patent cites more case studies. This is encouraging for AA patients — especially given it seems confer benefit even in more severe cases, of which are generally more likely to be resistant to treatment.

But it bears repeating: even Dr. Brotzu has claimed it’s difficult to know just how effective the lotion is for AA – mainly because of the spontaneous recoveries.

Helminthic therapy

Helminths, better known as hookworms, are tiny parasites that embed themselves in the small intestines of their hosts.

Helminths are unique in that they have a novel survival mechanism — one that might actually to a broader, modulatory effect on the whole immune system!

The specifics? Helminths “mute” the activity of T-cells, protecting them from destruction by the host’s immune system. This is accomplished through the stimulation of Tregs, a group of cells that reduce the inflammatory potential of the immune system.

As such, in theory, T-cell activity is modulated as a whole, reducing our reactivity to other reactive compounds — including our own tissue. Because auto-reactivity to our own tissue is what mediated autoimmunity (including in AA) reduced T-cell activity may also mean a reduced risk of autoimmunity.

And though research on helminth therapy is still in its infancy, preliminary studies suggest that this evidence might just translate to real-world efficacy. In fact, the therapy has shown promise for a variety of disorders, ranging from inflammatory bowel disorders to allergy all the way to mouse models of multiple sclerosis, an autoimmune disorder.

Considering this evidence, it’s not surprising that Moises Velasquez-Manoff, a male with alopecia totalis, reported hair growth for the first time in years following his experimentation with helminth therapy. He details his experience with helminth self-infection, alongside a historical perspective of helminth eradication, in his book: An Epidemic of Absence.

While this evidence alone is certainly not enough to warrant self-experimentation with helminth self-infection, this emerging research is compelling and underscores the growing importance of the symbiotic relationship of humans and microbes.

Success rates

As seen in the outcomes of the different studies, the likelihood of significant (or complete) recovery is relatively high. And, again, a large proportion of AA patients (34-50%) will spontaneously recover within one year.

This is great news! But, it also makes it difficult to effectively estimate the true success rate of treatments. So, is there any way that someone with AA might be able to gauge their likelihood of recovery (or lack thereof)?

Yes. In clinical practices, there are criteria for AA known as “poor prognostic factors” – i.e., things that might make you less likely to experience full hair recovery. According to the literature, these include:

1. Bald patches that persist for longer than 1 year.
2. Onset of hair loss before puberty.
3. A family history of AA.
4. Ophiasis pattern of AA.
5. Associated nail changes, a.k.a when nail changes occur alongside AA.
6. Atopy, a.k.a a propensity to developing allergic diseases like eczema, asthma, and allergic rhinitis.

So, if you fit into these categories, chances are your AA might be more treatment-resistant. That being said, it doesn’t mean you can’t recover your hair; it just means that you may need to explore more treatment avenues (or combination therapies) to find what works for your hair loss specifically. Your practitioner can help guide you through identifying these treatment avenues.

With that, you’ll also want to consult your doctor early into the process – as treatment resistance can increase as the condition progresses. As such, it’s better to forego experimental / home remedies and begin a treatment plan right away.

This isn’t to say natural therapies might not be an option for you, but, rather that you should discuss the evidence of those treatments with your doctor and, if suited to you, explore the therapy under their supervision.

This will help avoid treatment resistance that may result from delayed treatment, which would partly mitigate a major poor prognostic factor that is within your control.

Summary

Alopecia areata (AA) is a form of autoimmune hair loss characterized by inflammation, exclamation mark hairs, patchy hair loss (in early stages), and hair follicle miniaturization (in later stages). The condition can progress to alopecia totalis (loss of eyebrow and eyelash hairs) or alopecia universalis (loss of hair all over the body). But in many cases, it spontaneously reverses.

An autoimmune attack near the hair follicle stem cell bulge is what triggers AA-related hair loss. This results in inflammation, stem cell dysfunction, a malformed hair follicle, and thereby thiner, brittler hair that is prone to breakage. Eventually, hair cycling also becomes dysfunctional, leading to continued hair growth dysfunction and premature hair fall.

Thankfully, a large proportion of AA cases will spontaneously resolve within a year of onset. Having said that, it’s not a guarantee. So, while “waiting it out” may mean you need no treatment at all, it also poses a risk of progression. The further AA progresses, the higher the likelihood of treatment resistance.

So, it’s important that talk to your doctor when you first notice the hair loss. The earlier you catch it, the better your chances of regrowth. This is especially true if:

• Your hair loss began before puberty
• You have a family history of AA.
• Your hair loss is in the “ophiasis” pattern.
• Your hair loss is associated with nail changes.
• You have concurrent atopy (eczema, asthma, allergic rhintis).

Nevertheless, a wide array of treatment options do exist — both drug-based and non-drug-based – for manageable and refractory cases alike. Generally, corticosteroids are one of the first-line treatments. When corticosteroids aren’t effective, immunotherapy, methotrexate, JAK inhibitors, and alternative treatments (aromatherapy, vitamins/minerals, microbial modulation, and more) are usually explored.

Overall, the prognosis for most AA patients is good. Having said that, the risk of relapse is still high. This is mainly attributed to the fact that most treatments are confined to suppressing the signaling that leads to AA hair loss, as opposed to mitigating the root cause of AA. We just don’t know enough about the origin of AA to target these causes (yet).

The one exception to this rule might be fecal microbiota transplants (FMT) — a treatment that has shown major hair recoveries for long-standing AA patients (who typically don’t respond well to treatment), and no signs of relapse for those responders (at least within study windows of 1.5 to 3 years). However, evidence on FMT is incredibly limited. Moreover, the treatment is currently not readily accessible in the US (unless you have AA and you’re seeking treatment for a chronic C. difficile infection).

Overall, hair regrowth is absolutely possible for most AA patients — whether through natural or conventional means. Just make sure to get in touch with a doctor as soon as you notice your hair loss, so that they can help direct a treatment plan that’s going to be best suited to your condition.

If you have any questions, please feel free to leave them in the comments!

Scarring alopecias make up about 7% of patients seen in hair loss clinics. This means almost 1 in 10 hair loss cases are attributed to scarring alopecia.

In this article, we’ll outline what scarring alopecias are, what makes them unique, and why they might develop. Then we’ll uncover why this classification of hair loss – scarring vs. non-scarring – might be a bit outdated.

Finally, we’ll reveal new research that’s changing the way we think about scarring forms of hair loss. Historically, scarring alopecias have been considered irreversible. But new case reports are showing just the opposite: that some people with scarring alopecias can achieve significant – and sometimes complete – hair regrowth.

We’ll dive into why this is important, how this may impact treatment avenues, and what you can do to start combatting the progression of scarring alopecias today, both naturally and conventionally.

What are scarring alopecias?

Scarring alopecias are an umbrella term for hair loss from the rapid destruction and scarring of hair follicles.

There are several types of scarring alopecias (1), and each type varies by its presentation and causes:

• Central centrifugal cicatricial alopecia (CCCA). A type of hair loss that occurs predominantly in African American women. Characterized by a progressive thinning that begins in the center of the scalp and gradually expands to the peripheral regions. The only feature that distinguishes it from female pattern hair loss is the lack of visible follicles in the affected areas and a shiny, smooth scalp. It was once believed to be caused by hair styling techniques; however, recent data (2) has refuted that claim.
• Frontal fibrosing alopecia. This type of scarring alopecia occurs in a band-like distribution in the front of the hair and may also be present in the eyebrows. It mostly affects postmenopausal women. It predominantly affects the hairline, leading to uniform recession as if the hairline marched backward.
• Lichen planopilaris. Patchy hair loss with itchiness, scaling, and visible redness in affected areas. It might also affect non-scalp areas. It sometimes presents as diffuse thinning.
• Chronic cutaneous lupus erythematosus. Patchy, scarring hair loss as a result of an autoimmune disorder: lupus. Onset of this type of scarring alopecia may result from UV exposure, though research hasn’t yet confirmed this.
• Pseudopelade of Brocq. Small and/or large irregular patches of hair loss with no signs of inflammation.
• Folliculitis decalvans. A single patch of hair loss that progressively expands. Typically found on the peripheral regions of the scalp. Affected areas may have pustules, honey-colored crusting, and tufting.
• Dissecting cellulitis of the scalp. Multiple, red, inflamed, and interconnected nodules that erupt from various scalp regions in somewhat of a web-like pattern. It may also be associated with acne conglobota.

How do scarring alopecias happen?

No one is quite sure. However, many researchers believe scarring alopecias are caused by an interaction between inflammation, our immune systems, and (potentially) our hormones.

Similar to other hair loss disorders, the step-process for developing a scarring alopecia seems to be:

Inflammation >> scarring >> hair loss

You might see this step-process and think it looks a lot similar to other hair loss disorders, like androgenic alopecia (AGA). At face-value, you’re right. But there are a few differences that make scarring alopecias unique.

1. In scarring alopecias, the location of inflammation is in the hair follicle stem cell bulge; in androgenic alopecia, it’s in the infundibulum (upper third of the hair follicle) and likely deeper below the hair follicles, but above the galea aponeurotica.
2. In scarring alopecias, the nature of inflammation in unknown and/or autoimmune-related; in androgenic alopecia, the inflammation is likely related to scalp tension, pathogenic microorganisms, and accelerated hair cycling.

It might seem absurd to distinguish scarring alopecias from androgenic alopecia by the nature and location of inflammation. After all, our hair follicles are already tiny “mini-organs”. What difference does it make if one hair loss disorder’s source of inflammation is just a couple of nanometers away from another’s?

Apparently, a lot. And this is because across hair loss disorders, the location of inflammation predicts where scarring will occur, which predicts what these hair loss disorders will end up looking like.

This is why, in the later stages, androgenic alopecia and scarring alopecias look so different:

With scarring alopecias, the inflammation is far more widespread, so the scarring ends up wiping out the entire hair follicle – the stem cell bulges, sebaceous glands, arrector pili muscles, and hair shaft.

In androgenic alopecia, the scarring remains clustered around the hair follicle. Subsequently, the scarring doesn’t wipe out these other components of our hair follicles until many years into AGA’s progression.

In scarring alopecias, why do a hair follicle’s stem cell bulges become inflamed?

No one is quite sure. While researchers have identified dozens of potential triggers (3) across patients with scarring alopecias…

• Sebaceous gland dysfunction
• Substance P transmission (a neuropeptide released during stress)
• Deficiency in PPAR signaling
• Collapse of hair follicle immune privilege (the hair follicle is generally resistant against to damage by the immune system)
• Bacterial infection
• Abnormal cellular changes
• Genetic factors
• Hairstyling
• Certain drugs (anticonvulsants, hepatitis B vaccine, cyclosporin)
• Autoimmunity
• Sunscreen use on the forehead

…It’s still unclear which causes might apply to each case, why our hair follicle’s stem cell bulges become inflamed, and why this inflammation becomes persistent in the first place.

It all seems to begin with a miscommunication between an inflammatory stimulant, our immune systems, and our hair.

The miscommunication: inflammatory stimulants, myofibroblasts, and beyond

During a normal inflammatory process, the body encounters some sort of inflammatory stimulus – a wound, a virus, or even an environmental irritant. This stimulus is identified by the immune system as foreign, at which point our immune system recruits cells to “attack” the foreign invader. This leads to inflammation (i.e., tissue swelling), which in many cases, is enough to kill off the foreign invader. Once the threat is gone, the immune system signals these cells to stop attacking, and the inflammation dissipates, leaving us the same as we were prior to the attack.

In scarring alopecias, this process does not go according to plan.

During scarring alopecias, our immune system picks up on a foreign threat and sends a group of cells called myofibroblasts to start attacking. These myofibroblasts have a number of roles in the body – three of which are (1) enhancing the inflammatory response, (2) supporting the healing process, and (3) producing proteins like collagen (which, if produced in a disorganized fashion, form the building blocks of scar tissue).

Under normal settings, myofibroblasts would help enhance the inflammatory response until the foreign threat is destroyed, at which point the myofibroblasts would no longer be needed. At this point, the myofibroblasts would then help to repair the damage caused by inflammation by laying down new collagen fibers (i.e., skin tissues). Then, these myofibroblasts would die off.

However, in the case of scarring alopecias, myofibroblasts fail to die off. To put it simply, there’s a disruption in the normal cell signaling that tells our myofibroblasts that they’re no longer needed. As a result, they continue to lay down collagen, which becomes excessive and disorganized, which then turns to scar tissue.

Subsequently, functional tissue begins to be replaced by poorly-functioning scar tissue. As the fibrosis continues, the affected organs continue to lose functionality. We see this in conditions like cirrhosis, scleroderma, and pulmonary fibrosis (fibrosis of the lungs) – for example, where fibrosis makes it difficult for the liver, skin, and lungs to do their job.

This is exactly what happens in the hair follicle during scarring alopecia.

Infection and sustained inflammation begin to severely damage the hair follicle. And unfortunately, this scarring process ends up destroying our hair follicle stem cell bulges. This stem cell bulge is incredibly important; it contains the “blueprints” – or the building blocks – of each hair follicle. And without a hair follicle stem cell bulge, our hair follicles have no blueprints to follow for replication.

This leads to the complete destruction of the hair follicle… and the scarring of its surrounding skin. And as you can imagine, this is not a position most hair loss sufferers want to be in.

Are scarring alopecias reversible?

Traditionally, researchers have generally held the stance that scarring alopecias aren’t reversible.

This is because of the fact that scarring alopecias (1) lead to widespread scarring of an entire skin region, and thereby (2) wipe out the hair follicle stem cell bulges. For these reasons, many researchers have held onto the belief that scarring alopecias are irreversible – and that the best we can do is slow or stop their progression.

Encouragingly, this belief is now changing. Why? Because new evidence is showing that scarring alopecias are not only theoretically reversible, but that we actually have case studies of this happening. It’s all a matter of unlocking how to do it on a consistent basis.

Here’s why we believe this is possible.

#1: AGA, which also leads to scarring, is reversible even in its latest stages.

To reiterate from earlier, end-stage AGA closely resembles that of end-stage scarring alopecias. In both conditions, we see so much fibrosis (scarring), that there’s a total loss of follicular integrity.

Having said that, even in late stages of androgenic alopecia, we’ve seen pretty significant hair regrowth. This is obvious with examples from a few of our case studies from our membership community – like Mike and Raul – who used natural methods to see regrowth beyond what is typically observed with conventional treatments.

Mike’s Regrowth

Raul’s Regrowth

But perhaps the most impressive example of hair regrowth from advanced AGA happened entirely by accident.

In 1986, a 78-year man who’d been bald for 30+ years fell asleep in his rocking chair. Inadvertently, he slumped over, landed head-first onto hot coals, and received second degree burns across much of his scalp.

He refused to be treated at the hospital and was eventually sent home as an outpatient. Four months later, he returned for a checkup. During that time from the injury, he’d accidentally regrown his entire juvenile hairline (4).

Remember: in advanced cases of AGA, a hair follicle’s stem cell bulges appear either scarred or completely depleted. This implies an inability for hair recovery. Yet here, we see a case of complete hair recovery… just the opposite of what we’d expect.

And as we dig deeper into the research on scarring alopecias, we can find plenty of cases where recoveries happen, too.

#2: scarring alopecias have been reversed before!

There are several case studies of people with scarring alopecias regrowing significant amounts of hair. In some cases, the hair recovers completely.

In some cases, this has happened with interventions as simple as stopping the use of facial sunscreen (5). In other cases, significant regrowth came after using topical metformin (6). In one case of lupus-related scarring alopecia, complete hair regrowth was observed within three months following the use of hydroxychloroquine (7). And in cases of frontal fibrosing alopecia, oral finasteride led to near-complete hairline regrowth after just 12 months (8).

In light of these findings, there are really only two explanations:

1. In scarring alopecias, stem cell bulges aren’t totally lost. Therefore, the hair is still recoverable. Or…
2. Our understanding of hair follicle stem cell bulges needs to be revised. Maybe hair follicles can regenerate in the absence of stem cells, and through not-yet-discussed processes, like that of follicle-to-follicle communication.

Let’s explore that second idea for a second, as it may shape the next decade of hair loss research.

What do we know about follicle-to-follicle communication?

Follicle-to-follicle communication is a phenomenon that was originally observed in one fascinating study (9) – the findings of which we described in this article. To summarize:

In 2015, researchers wanted to see if hair follicles could communicate with each other to coordinate behaviors – like making new hair follicles. So they set up a test…

They plucked 200 hairs from the backs of mice… but did so while controlling for the diameter of a plucking region. In some cases, 200 hairs were plucked in a 2.4mm region. In other cases, 200 hairs were plucked from an 8mm region. The smaller the region, the higher-density the plucking – and vice-versa.

The goal: to see if hair follicle behavior changed on how closely hairs were plucked from one another. So they measured hair growth over the next several weeks.

The results were fascinating.

With low-density plucking, hair follicles either didn’t grow back at all… or grew back to their normal pre-plucking densities. That’s what we would expect to happen.

But with higher-density plucking, additional hair follicles were created… to the tune of a five-fold increase.

What’s more interesting is why this happened. The researchers theorized that higher-density plucking created more inflammatory signaling, which led to more cross-communication between hair follicles directly next to each other, which signaled to hair follicles to start regenerating – regardless of whether they’d been plucked.

The end-result: a huge increase in hair.

The implications? That nearby hair follicles can communicate with one another (!), and that these communications must include signaling for hair follicle regeneration. Based on this study, it’s clear that healthy hair follicles can coordinate regeneration with damaged hair follicles.

So, how does this relate to scarring alopecia?

Considering hair loss from scarring alopecia is a result of complete hair follicle destruction, and considering that this destruction has puzzlingly reversed itself across many case studies…

We can presume that follicle-to-follicle communication is playing a role here, and that understanding this role (and harnessing this cellular crosstalk) is probably one way people with scarring alopecias can unlock huge hair recoveries.

So, how do we do this?

We don’t yet know! Research is still emerging, and as it continues to evolve, we’ll update this article.

In the meantime, there’s plenty we can do to stop the progression of scarring alopecias – and potentially even see major recoveries.

What are the current treatments for scarring alopecias?

Step 1: connect with a dermatologist

The first step is always making an appointment with a dermatologist. By understanding what kind of scarring alopecia you have, you can better target your treatment regimens to save yourself time, effort, and money.

Step 2: identify and remove any potential inflammatory “triggers”

Once you’ve scheduled your appointment, one of the most critical next steps is to make your best effort to identify and remove some of the most common triggers of scarring alopecias. This will be highly individual and dependent, again, on the type of scarring alopecia with which you’re diagnosed.

Here are a few of the common inflammatory stimulants suspected in scarring alopecias:

• Sunscreen use: there is a weak link between sunscreen use and frontal fibrosing alopecia (FFA) (5). Some researchers hypothesize this could be due to decreased sebum production during the time in which a woman is most likely to be affected by FFA, menopause. This results in an inability to clear topical products, like sunscreen, from the follicle, potentially leading to an autoimmune reaction. Other researchers have proposed an alternate view: with the anti-inflammatory, immunomodulatory effects of UV light, blocking UV light (using sunscreen) may actually encourage autoimmunity in the follicle. Cessation of sunscreen use has been shown to produce noticeable regrowth in as little as 6 months with an almost full recovery in 36+ months.
• Hairstyling: While studies have failed to establish hairstyling as the sole cause of CCCA, certain hairstyling techniques may contribute to at least some cases of scarring alopecia. If you find yourself dealing with a potential case of scarring alopecia and you regularly receive hair relaxant treatments, employ hot combing, or style your hair in braids, cornrows, or using other traction styling methods (10) – it might be best to avoid these treatments and/or stylings (or at least reduce their frequency) until you can rule out their potential involvement.
• Environmental toxins as inducers of autoimmunity: Autoimmunity is one of the purported causes underpinning the development of scarring alopecia. This is due to the fact that the stem cell bulge of the follicle is normally a site of immune privilege, meaning it is usually protected from the action of the immune system. However, autoimmune processes can actually cause this immune privilege to be lost. Interestingly, environmental toxins have the ability to induce autoimmunity. For this reason, avoidance of environmental triggers linked to autoimmunity, like rancid vegetable oils, mineral oils, and sources of heavy metals, is a good precautionary measure (11).
• UV exposure: Some causes of scarring alopecia, like chronic cutaneous lupus erythematosus, are exacerbated by UV exposure. Use of sunscreen or UV-blocking clothing/hats may be needed to prevent the worsening of lesions that contribute to hair loss.

Step 3: settle on a treatment approach

There are two ways we can approach this: drug-based treatments and non-drug treatments.

We’ve divided these interventions into their respective sections and described who these treatments might be best for, which dosages are used in the literature (where applicable), the outcomes of the research, and what potential issues might arise with each given treatment.

Drug-based treatments

Topical, intralesional, and oral corticosteroids:

• Best candidates: Most forms of scarring alopecia, patients with CCCA not related to traumatic hair styling.
• Dosages: 10mg/mL for intralesional injections every 6-8 weeks; 25-40mg per day for 2-4 months with oral corticosteroids (1).
• Outcomes: Corticosteroid treatment, in any form of administration is mostly limited to halting the progression of disease as it doesn’t address the scarring that impedes hair follicle regeneration. Can promote regrowth in some patients with dissecting cellulitis (12).
• Problems: Oral corticosteroids are limited to severe/rapidly progressing disease; topical corticosteroid treatment can result in skin atrophy, a.k.a thinning of the skin.

Hydroxychloroquine:

• Best candidates: Patients with frontal fibrosing alopecia, lichen planopilaris, and chronic cutaneous lupus erythematosus.
• Dosages: Below 7.5/mg/kg for lichen planopilaris and frontal fibrosing alopecia, 400mg daily during summer months with chronic cutaneous lupus erythematosus and smaller doses during winter (1).
• Outcomes: Effective at decreasing signs and symptoms of lichen planopilaris and frontal fibrosing alopecia and preventing further hair loss, effectively resolve lesions related to chronic cutaneous lupus erythematosus (13), full hair regrowth has been observed with hydroxychloroquine in at least one case of lupus-related alopecia (7).
• Problems: Studies are often too short to estimate the true incidence of retinopathy at dosages used for these conditions.

Antibiotics (Minocycline, rifampicin, fusidic acid):

• Best candidates: Patients with folliculitis decalvans.
• Dosages: 300mg rifampicin 2x daily (should not be used as a monotherapy, which can promote antibiotic resistance), combination of 300mg rifampicin, 300mg clindamycin, and fusidic acid along with topical corticosteroid lotion for 3 months has been used with success, topical clindamycin or benzoyl peroxide can control mild cases, oral antibiotics are needed for more severe cases (1).
• Outcomes: Effective at addressing the infection that leads to folliculitis decalvans, but not restoring the hair lost.
• Problems: Rifampicin is the preferred antibiotic because it is highly lipid-soluble (the scalp environment is very lipidic) and accumulates in high quantities in the hair follicle, however, antibiotic resistance is a major issue with its use.

Topical metformin:

• Best candidates: Who topical metformin might be best for is still unclear, as research is preliminary, but case studies have demonstrated success in CCCA patients (6).
• Dosages: 10% topical metformin with the potential for higher concentrations if the patient responds well to the treatment.
• Outcomes: Although research is preliminary, there have been two cases of partial regrowth in CCCA – traditionally believed to be irreversible (and notoriously difficult to treat) (6).
• Problems: Preliminary research suggests there is little to no systemic side effects. Instead, side effects are usually superficial and limited to scalp dryness and irritation.

Oral Isotretinoin (Accutane®):

• Best candidates: Patients with dissecting cellulitis and cases of chronic cutaneous lupus erythematosus resistant to antimalarial therapies like hydroxychloroquine.
• Dosages: 0.5-1mg/kg daily for dissecting cellulitis (1).
• Outcomes: Usually produces rapid results in chronic cutaneous lupus erythematosus, treatment for 6-11 months in dissecting cellulitis shrinks lesions and can even induce periods of long remission.
• Problems: Oral isotretinoin can cause large quantities of hair follicles to prematurely enter the telogen phase, which can lead to diffuse shedding (1). The risk of disease progression should be weighed carefully against the potential risk of increased shedding.

Finasteride:

• Best candidates: Patients with frontal fibrosing alopecia.
• Dosages: 2.5mg daily (14).
• Outcomes: Some studies suggest finasteride is the most effective therapy for treating frontal fibrosing alopecia. Patients with this condition can expect a response rate of about 50% with finasteride alone (14). At least one case report demonstrated marked regrowth and a reversal of skin atrophy (i.e., skin thinning) (8).
• Problems: In women with already low or normal androgen levels, finasteride could produce sexual/mental side effects.

Non-drug treatments

Microneedling + platelet-rich plasma:

• Best candidates: Unknown.
• Methods: 20 sessions spaced 2 weeks apart.
• Outcomes: Clinical improvement in one case of general scarring alopecia – the details of this clinical improvement aren’t specified (i.e., improvement of inflammatory lesions vs. actual hair regrowth)
• Problems: Likely cannot be used to treat some forms of scarring alopecia like folliculitus decalvans, at least in their active infection phase, due to the bacterial nature of the condition.

Low level light/laser therapy (LLLT):

• Best candidates: Patients with lichen planopilaris.
• Methods: 272 pulsed laser diode cap with 1360 mW total output
• Outcomes: Case reports suggest lichen planopilaris patients may be able to achieve hair regrowth with the use of LLLT (15).

Excimer laser (UV-B light)

• Best candidates: Patients with lichen planopilaris and some cases of frontal fibrosing alopecia.
• Methods: Sessions as frequent as twice weekly with an average of 10 sessions reported in the literature.
• Outcomes: Studies have demonstrated a decrease in inflammation, as well as some instances of hair regrowth (16).

Hair Transplants

We know from the literature that there are some cases of scarring alopecia that are reversible. But, what if your hair doesn’t grow all the way back, even with the best-of-the-best treatment?

This is where hair transplants might be useful.

Hair transplants in scarring alopecias are different than hair transplants for non-scarring hair loss disorders. While grafts in non-scarring alopecias have a 90% survival rate, scarring alopecias may only have an average 50% survival rate.

But, transplants don’t have to be a stab in the dark. We can usually predict whether or not a transplant is going to be successful by (1) understanding what kind of scarring alopecia you have, and (2) performing a pre-surgery transplant test.

We’ve compiled the types of scarring alopecias that are more likely to see success from a transplant vs. those that might not:

Scarring alopecias more likely to receive transplants successfully	Scarring alopecias where hair transplants are less likely to survive
Central centrifugal cicatrial alopecia (CCCA)	Lichen planopilaris
Discoid lupus erythematosus	Frontal fibrosing alopecia
Pseudopelade brocq
Folliculitis decalvans

However, the safest way to estimate your individual tolerance to a hair transplant is to have a dermatologist perform a pre-surgery transplant test.

But, what if your chances of hair transplant survival end up being low? Or what if hair transplants are too expensive? Or too invasive? What are the options, then?

In these cases, there is one additional option.

Artificial hair integrations

For treatment-resistant and/or transplant-intolerant cases or for those who aren’t comfortable with the price or the procedure, the next best option is artificial hair integrations.

The good news is that these are inexpensive and readily accessible – and something you can begin to use right away. But, you’ll want to be absolutely sure that these integrations aren’t putting any additional strain on existing hair, as this can do more harm than good. In some cases, it may trigger a case of traction alopecia or, worse, a new case of scarring alopecia.

So, to recap, here’s a sequential approach you should consider for treatment:

1. Make a dermatologist appointment to identify what kind of scarring alopecia you might have (if any).
2. Identify and remove any potential triggers.
3. Based on what type of scarring alopecia you have, explore some treatment avenues provided and discuss them with your dermatologist.
4. If you aren’t able to achieve full recovery, explore hair transplants. Performing a pre-surgery transplant test can help you gauge whether or not a transplant will survive on your scalp.
5. If you are intolerant to transplants and/or aren’t comfortable with the price or the procedure itself, artificial hair integrations are relatively inexpensive and very accessible.

Summary

Scarring alopecias are relatively uncommon; they constitute just 7% of hair loss diagnoses in hair loss clinics. Having said that, they’re characterized by aggressive scarring. This scarring leads to the destruction of skin tissue surrounding hair follicles, as well as the destruction of stem cell bulges which make hair follicles and the hair follicles themselves. Consequently, many researchers have historically considered that scarring alopecias are irreversible.

This is no longer the case. Case reports of full hair recoveries from scarring alopecias, alongside evidence that healthy hair follicles and unhealthy hair follicles can actually communicate with each other, now leads researchers to believe that scarring alopecias are reversible… we just don’t know how to do it consistently (yet).

Because scarring alopecias are less common, there are still many questions researchers have yet to answer:

• Why are some cases of scarring alopecias reversible, if all scarring alopecias are believed to result in a loss of the stem cell bulge?
• If there are at least some scarring alopecias that happen to retain stem cells, could there be an overlap in treatments with AGA? In other words, could some scarring alopecia patients benefit from AGA treatments that address fibrosis?
• If stem cells aren’t retained, is there some other regenerative process, like follicle-to-follicle communication, at play?

As researchers attempt to answer these questions, there are still some great treatments out there for scarring alopecia patients – both drug-based and drug-free, that have shown clear benefit. While most are limited to improving symptoms and slowing or halting the progression of hair loss, some patients are seeing partial and/or full recoveries.

For those who find their hair loss is treatment-resistant or want to restore hair lost to scarring alopecia, hair transplants are a decent option. However, they can be a hit or miss, being that the transplant survival rate is around 50% (vs. 90% for other hair loss types). You can maximize your chances of survival by identifying what kind of scarring alopecia you’re dealing with as well as performing a pre-surgery transplant test.

Artificial hair integrations are also a great option — and one much cheaper and more accessible than hair transplants. However, it is of the utmost importance that these are applied correctly to avoid undue strain on healthy hair (which may trigger the onset of new hair loss).

Have any questions about the new treatments for or emerging research on scarring alopecia? Please let us know in the comments section below.

Oral minoxidil for women with hair loss: an underutilized treatment?

Although topical minoxidil seems to get most of the attention as a hair loss treatment, its oral counterpart is also effective at promoting hair regrowth in both males and females.

Generally, higher dosing means better efficacy, but with a higher risk profile. As it relates to oral minoxidil, this means limb swelling, low blood pressure, and, potentially, heart palpitations. But, there’s one side effect that may be more concerning for women taking oral minoxidil than men: excessive body hair growth.

Considering this is something most women want to avoid or may also struggle with alongside their hair loss (in cases of female androgenic alopecia), this side effect could be of significant concern.

So, is there a way we can harness the hair-growing effects of oral minoxidil without the side effects?

Yes. This Quick Win dives into the research: the clinical evidence, the best dosages, and the best ways to avoid excessive body hair growth while taking this medication.

Note: Quick Wins are short articles focused on answering one question about hair loss. Given their specificity, these articles are written in a more scientific tone. If you’re new to hair loss education, start with these articles.

Oral minoxidil: research at a glance

What is oral minoxidil?

Oral minoxidil was initially developed as a treatment for ulcers, but later rebranded as a medication that might potentially lower blood pressure. During clinical trials, a lot of participants started reporting unexpected hair growth. This led researchers to reformulate minoxidil as a topical for hair loss, which eventually became FDA-approved in 1988.

Minoxidil’s structure

While no one is quite sure how minoxidil works to regrow hair, researchers suspect that it has something to do with minoxidil’s ability to (1) improves blood flow, and (2) increase prostaglandin E2 synthesis – a fatty acid derivative that likely plays a role in hair cycle maintenance.

Is oral minoxidil better than topical minoxidil?

Potentially. Both oral and topical minoxidil need to interact with an enzyme called sulfotransferase before becoming active and eliciting any effects on our hair follicles. Unfortunately, many men and women who are losing their hair also lack enough sulfotransferase in the scalp skin for topical minoxidil to do its job. This likely explains why for 30-40% of people, topical minoxidil doesn’t work at all (myself included).

Enter oral minoxidil. This drug is metabolized is activated in the liver – where there is plenty of sulfotransferase to go around – and then rapidly distributed to tissues throughout the body. This is why, when it comes to regrowing hair, oral minoxidil has a much higher response rate – typically 90-100%.

Unfortunately, with the rapid tissue distribution of oral minoxidil, we can also experience its hair-growing effects elsewhere in the body: namely, across our chests and faces.

This isn’t such a problem for men (in fact, many men enjoy the increased body and facial hair growth). But for women, this can be a dealbreaker – with the fear of unwanted body hair growth relegating them topical minoxidil or other treatment options.

So, for females, is there a way to mitigate any unwanted side effects of oral minoxidil while still maximizing its hair-promoting effects?

Yes.

Clinical studies

Unlike the research on topical minoxidil, oral minoxidil research is sparse (especially in women). Nevertheless, there do seem to be certain dosages of oral minoxidil – and combination therapies – that greatly reduce the risk of unwanted hair growth in women.

Here’s a table of the studies conducted on women taking oral minoxidil for hair loss.

Daily Dose (duration)	Type of Hair Loss	Results	Side Effects
1mg daily (6 months) (1)	Female Pattern Hair Loss	12% increase in hair count	Limb Swelling: 4% Hypotension: 0% Excess Hair Growth Outside the Scalp: 27%
0.25mg + 25mg spironolactone daily (12 months) (2)	Female Pattern Hair Loss	72% improvement in hair loss severity	Limb Swelling: Not reported Hypotension: 2% Hives: 2% Excess Hair Growth Outside the Scalp: 4%
0.25mg-2.5mg with most patients taking 1mg (12 months) (3)	Chronic Telogen Effluvium	45% improvement in hair loss severity	Limb Swelling: Not reported Hypotension: 5% Excess Hair Growth Outside the Scalp: 38%

Looking at the results, we see that all doses of oral minoxidil are effective at promoting hair growth: 1.5-2 mg by itself, and 0.25 mg of oral minoxidil in combination with 25 mg of spironolactone (an anti-androgen drug).

When analyzing side effects, serious adverse events – like hypotension and limb swelling – are uncommon, even with doses as high as 1-2.5mg. But at these dosages, there are quite a few women (27-38%) reporting unwanted hair growth elsewhere on the body… which is exactly what we’d like to avoid.

But there’s an inflection point: a dosage that we can minimize the risk of unwanted hair growth (hypertrichosis) while maximizing oral minoxidil’s pro-hair effects on the scalp.

It’s with 0.25mg of oral minoxidil + 25mg of spironolactone daily.

With this daily dosage of oral minoxidil + oral spironolactone,  only 4% of women report excess hair growth… while the majority of females in the study saw significant improvements to their scalp hair loss.

What this means: this combination therapy of low-dose minoxidil + low-dose spironolactone (an anti-androgen drug) is sort of the oral minoxidil “sweet spot” – at least in terms of lowering your risk of body hair growth, and raising your likelihood of scalp hair growth.

Low-dose oral minoxidil + low-dose oral spironolactone is a winning formula for female hair loss sufferers

But, what if you’re sensitive to spironolactone?

Although 0.25 mg of oral minoxidil alongside 25 mg of spironolactone daily might be a viable option for many women with hair loss, spironolactone can cause mild allergic reactions in sensitive individuals. (4, 5) While these effects are rare, we have had some members of our community echo these concerns and even report adverse reactions of their own.

So, maybe you’ve found that you’re sensitive to spironolactone and that combining low dose spironolactone + oral minoxidil isn’t an option for you. What’s the next best option?

At this point, it really depends on what your tolerance for higher dosages of oral minoxidil (and their potential for side effects). Higher doses of 1mg to 2.5mg will likely provide results, but also increase your risk of body/facial hair growth.

If you have milder hair loss or really aren’t comfortable with increased body/facial hair (or don’t want to manage it with other therapies), you can always start with 0.25mg of minoxidil on its own. If it still isn’t providing the results you’re looking for, you can always look into alternative oral or topical therapies to bolster your results. As always, discuss your options with your doctor before doing anything.

You may also decide to implement totally different therapies. After all, many females have seen success treating hair loss outside of the drug model, and with therapies like:

• Platelet-rich plasma
• Massaging
• Microneedling
• Low-level laser therapy

…and more. So, before you jump on any treatment, make sure that you have a firm understanding of 1) the drivers of your hair loss, and 2) your treatment options. Then, make an action plan for hair recovery that’s tailored to your needs and preferences.

What’s the bottom line?

If you’re a female with pattern hair loss, and your goal is to maximize the hair-promoting properties of oral minoxidil while minimizing your risks of hypertrichosis, research shows that combining 0.25mg of oral minoxidil with 2.5mg of spironolactone is likely your best option. At these dosages, you’re positioning yourself for scalp hair growth while minimizing the risk of body hair growth.

If spironolactone isn’t an option for you, that’s okay. Higher doses of oral minoxidil (1-2.5mg) don’t present with any increased risk of hypotension or limb swelling, but at these dosages, 27-38% of women do report excess body/facial hair growth in clinical studies. If this is a concern for you, consider combining low-dose oral minoxidil with alternative therapies or opting for another treatment altogether.

Lastly, oral minoxidil is a prescription medication. So be sure to consult your doctor before doing anything.

Question? Comments? Please reach out in the comments section.

Saw palmetto for hair growth: does it stack up to finasteride?

Saw palmetto is often touted as nature’s finasteride. This herbal extract reduces levels of the hormone dihydrotestosterone (DHT). For this reason, it’s clinically demonstrated to improve hair growth in men with androgenic alopecia (AGA).

But is saw palmetto as effective as finasteride?

Not quite. In fact, a closer look into the research on saw palmetto reveals that taking this supplement also comes with risks.

That’s not to say that saw palmetto is ineffective. But if you’re going to opt for saw palmetto over finasteride, you’re going to want to weigh its benefits and risks. Specifically, you’re going to want to know how saw palmetto compares to finasteride in terms of its (1) ability to reduce DHT, (2) ability to regrow hair, and (3) reported side effects.

This Quick Win dives into the details (and answers). The bottom line: saw palmetto isn’t as powerful as finasteride, but it also comes with some upsides that may make it a better option, at leaast for certain hair loss sufferers.

Note: Quick Wins are short articles focused on answering one question about hair loss. Given their specificity, these articles are written in a more scientific tone. If you’re new to hair loss research, start with our long-form articles.

What is saw palmetto?

Saw palmetto is a palm plant native to warm humid climates (Florida).

Saw palmetto plant

Thirty years ago, researchers discovered that certain polyphenol and lipid extracts of saw palmetto could reduce the activity of type II 5-alpha reductase – an enzyme our bodies use to make the hormone dihydrotestosterone (DHT).

DHT is the main hormone implicated in pattern hair loss, also called androgenic alopecia (AGA). And interestingly, the popular hair loss drug finasteride (Propecia®) reduces that same enzyme – type II 5-alpha reductase – to lower DHT levels and improve pattern hair loss outcomes in ~80% of men trying the drug.

Unfortunately, finasteride use is also associated with sexual side effects. This scares a lot of men away from trying the drug. It also leads many of them to wonder…

“If I use saw palmetto instead of finasteride, can I still regrow hair while also reducing my risk of side effects? After all, saw palmetto is natural, and natural often means safer.”

For starters, anything branded as “natural” isn’t always safer. Many natural supplements sold through Amazon and tested by third parties have been found to contain dangerous levels of heavy metals. Moreover, many popular natural extracts – i.e., green tea extract – have been associated with hepatic failure due to the metabolic demands these extracts can place on our livers. (For more information, see my master class).

In any case, if we’re to answer the question, “Is saw palmetto as effective as finasteride?”, we’ll need to evaluate saw palmetto versus finasteride in terms of its (1) expected hair regrowth, and (2) risk of side effects.

The rest of this Quick Win does just this.

Saw palmetto vs finasteride: hair regrowth

“Hair regrowth” is a non-specific term, and most clinical studies on pattern hair loss define this term differently:

• Reductions to hair shedding
• Improvements to anagen:telogen ratios
• Increases in non-vellus hair counts
• Global photography assessments

…the list goes on.

That’s why, whenever we’re diving in studies on hair loss, we standardize the term “hair regrowth” into two categories:

1. Response Rate. This is the percentage of people receiving treatment who see a slowing, stopping, or reversal in their hair loss. After all, simply slowing down the progression of AGA is a win for most hair loss sufferers.
2. Regrowth Rate. This is the percent change in terminal (i.e., non-vellus) hair counts before and after treatment. We use this metric because it’s best out there in terms of translation to visual improvements. Increases to vellus hair counts (i.e., small, wispy, white hairs) just don’t show up in photographs, so we don’t count those.

So, if we summarize the data on saw palmetto versus finasteride, how do these two interventions compare? (1) (2)

	Saw Palmetto (320mg)	Finasteride (1mg)
Response Rate	60%; dependent on the dose and delivery (supplement or topical)	80-90%
Regrowth Rate	0-10%; potentially higher if used alongside other therapies	10%, alongside thickening of miniaturizing hair

The key takeaway: compared to finasteride, saw palmetto has a lower response rate and regrowth rate. And when we look at the individual studies that constitute these aggregated estimations, things look a little bleak.

To date, there’s only one clinical study directly comparing saw palmetto versus finasteride for the treatment of androgenic alopecia. The investigation team randomized 100 men with androgenic alopecia into two groups. They gave one group 320mg of saw palmetto and the other group 1mg of finasteride – every day, for two years. (3)

The results? After 24 months, 68% of finasteride users saw hair regrowth, while only 38% of men taking saw palmetto saw hair regrowth. Moreover, investigators noted that in the saw palmetto group, hair regrowth only occurred in the crown (i.e., vertex), and that the magnitude of regrowth was significantly less than finasteride.

In other words, saw palmetto achieves half the response rate of finasteride, and that if regrowth does occur, it’s not nearly as impressive as what finasteride achieves.

Having said that, it’s not all bad news. That same study also demonstrated that 45/50 men in the saw palmetto group saw a stop in hair loss over the two years that they took it. So, in this one study, saw palmetto showed a response rate of 90%.

This means it’s not a complete stretch to say that most men taking 320mg of saw palmetto daily should see an improvement in their pattern hair loss. It’s just that this improvement won’t be anywhere near on-par what is achievable with finasteride.

Why isn’t saw palmetto as effective as finasteride?

This likely has to do with the ways in which saw palmetto reduces DHT, and the amount of DHT that saw palmetto reduces.

Finasteride is a synthetic azosteroid. It reduces DHT by competing with (and binding to) a coenzyme that our bodies use to make type II 5-alpha reductase – the enzyme that converts free testosterone into DHT.

Conversely, saw palmetto competitively and non-competitively inhibiting type II 5-alpha reductase, reducing the binding of DHT to androgen receptors, and increasing the conversion of DHT to a weaker metabolite called androstanediol (4).

The long-story short is that these factors, along with differences in the half lives of both finasteride and saw palmetto, lead to differences in their abilities to lower DHT.

For reference, see this graph on the DHT-reducing capabilities of both saw palmetto and finasteride, as organized by different tissue sites.

The bottom line: saw palmetto is about half as effective as finasteride because it just doesn’t reduce as much DHT.

What about side effects?

At this point, we’ve really only evaluated half of the question: is saw palmetto as effective as finasteride?

In terms of response rates and regrowth rates, the answer is no. But can saw palmetto make up for its lower efficacy by being a safer long-term supplement for hair loss sufferers?

Maybe.

Saw palmetto: risk of adverse events

Long-term clinical studies show that saw palmetto’s overall rate of side effects is just 2%. Moreover, if side effects do occur, they’re relegated more so to gastrointestinal distress than to sexual dysfunction. Even better, many studies on saw palmetto show no change in libido; some studies show improvement to sexual health (at least for men with enlarged prostates). (5) (6) (7)

Finasteride: risk of adverse events

The “Yelp effect” is a phenomenon where patrons of a business are far more likely to leave a review if their experience was negative rather than positive. Finasteride is a drug that suffers from the Yelp effect, meaning that its sexual side effects are often overstated and amplified online.

Having said that, side effects do occur. Moreover, the self-assessment questionnaires filled out by participants in large-scale clinical trials for finasteride were worded in such a way where under-reporting certain side effects were more likely than not (but that’s for another article).

In any case, finasteride use does come with a heightened risk of side effects. Depending on which study you cite, between 1% and 25% of finasteride users will report issues ranging from brain fog to depression to sexual dysfunction. (8) (9) Moreover, when side effects are reported, they seem to be of higher magnitude versus saw palmetto.

The bottom line:

• Finasteride’s side effects are likely overstated online and understated in the literature
• Compared to saw palmetto, finasteride likely leads to side effects that are (1) of higher incidence, and (2) more severe

Saw palmetto or finasteride: which one is right for you?

It depends on your risk tolerance for side effects, and whether you plan on combining saw palmetto with other treatments, therapies, or procedures to make up for its lower response rates and regrowth rates.

There’s evidence that supplemental + topical saw palmetto, alongside other ingredients, might lead to better hair loss outcomes than just supplemental saw palmetto. Moreover, combining saw palmetto with massaging, microneedling, platelet-rich plasma therapy, or other interventions might help mitigate its lower efficacy.

Having said that, making these choices will depend entirely on someone’s needs, preferences, and unique hair loss situation.

Anything else to know?

Unlike finasteride, saw palmetto isn’t standardized. Serenoa repens growing conditions, extraction methods, and manufacturing practices can all impact the composition, bioavailability, and absorption of each saw palmetto supplement. In fact, these differences might explain the variances in response rates and regrowth rates seen across saw palmetto studies.

So, if you’re looking for a more comprehensive guide on how to use saw palmetto – including recommendations for dosages, extraction practices, and combinations therapies – see our saw palmetto ultimate guide here.

The bottom line

In order to evaluate whether saw palmetto is as effective as finasteride, we need to understand how the supplement compares in terms of (1) response rates, (2) regrowth rates, and (3) risk of side effects.

Saw palmetto isn’t as effective as finasteride in terms of its response rates or regrowth rates, but it also seems to cause fewer (and less severe) side effects. Because of this, making the choice to use saw palmetto over finasteride depends entirely on someone’s risk tolerance for side effects, as well as whether they plan on combining the supplement with other treatments, therapies, or procedures to make up for its less-impressive efficacy.

	Saw Palmetto (320 mg)	Finasteride (1 mg)
Response Rate	60%; dependent on the dose and delivery (supplement or topical)	80-90%
Regrowth Rate	0-10%; potentially higher if used alongside other therapies	10%, alongside thickening of miniaturizing hair
Side Effects	2%; more relegated to gastrointestinal distress than sexual side effects	1-25%; partly psychosomatic, but more severe than saw palmetto

Otherwise, if you have any questions, please feel free to leave them in the comments section.

 

Ketoconazole shampoo is an anti-fungal, anti-inflammatory shampoo that is sometimes used to treat androgenic alopecia (AGA).

There are two formulations of ketoconazole shampoo: 1% and 2%. While 1% ketoconazole is sold over-the-counter as an ingredient in many hair loss shampoos, only 2% ketoconazole is clinically shown to improve pattern hair loss. And unfortunately, 2% ketoconazole requires a prescription from your doctor.

This leads a lot of pattern hair loss sufferers to opt for 1% ketoconazole shampoo, and mainly out of convenience. But if you’re opting for 1% ketoconazole instead of 2%, are you selling yourself short any potential hair gains?

More specifically, when it comes to 1% versus 2% ketoconazole for hair loss, does one percentage point really matter?

This Quick Win dives into the studies on ketoconazole to answer this question.

Note: Quick Wins are short articles focused on answering one question about hair loss. Given their specificity, these articles are written in a more scientific tone. If you’re new to hair loss education, start with these articles.

Is 2% ketoconazole better than 1% ketoconazole?

Currently, there are no studies directly comparing 1% to ketoconazole to 2% ketoconazole in their ability to promote hair growth.

However, we can look at some different studies that use either formulation and compare how each one performs in its respective studies. Then, we can compare the results of each study to get a feel for which one is more effective.

First, let’s look at 2% ketoconazole. This study investigated 2% ketoconazole’s ability to increase hair counts in AGA patients. They found that, after 6 months (and 3x per week of use), participants experienced an average 18% increase in hair count.

Now, let’s evaluate 1% ketoconazole. This study looked at the effectiveness of 1% ketoconazole for AGA. After 6 months of use 3x per week, 1% ketoconazole didn’t increase hair count, but it did decrease hair shedding. In other words, 1% ketoconazole is effective enough to slow or stop shedding, but not to promote hair regrowth.

Both studies employed the same frequency for the same amount of time and on subjects with the same condition. Because of this, we can assume that ketoconazole at a 2% concentration is likely more effective than at 1%.

An additional study also compared 1% versus 2% ketoconazole in their ability to combat the scalp yeast Malassezia and the condition seborrheic dermatitis. Malassezia overgrowths and seborrheic dermatitis are often observed alongside pattern hair loss. These conditions lead to excessive sebum production and scalp flaking (i.e., dandruff), and thereby may accelerate AGA by increasing overall scalp inflammation. Moreover, there’s also research suggesting that resolving Malassezia overgrowths and seborhheic dermatitis may enhance hair regrowth. Long-story short: if we’re going to use a ketoconazole formulation for hair loss, it only benefits us if that formulation also improves these conditions.

The findings from that research team? When it came to decreasing Malassezia load and scalp flakiness from seborrheic dermatitis, 2% ketoconazole outperformed 1% ketoconazole in both categories. Moreover, 2% ketoconazole led to fewer relapses of either condition.

“During follow-up [ketoconazole] 2% showed a trend to fewer relapses than [ketoconazole] 1%. [Ketoconazole] 2% had superior efficacy compared to [ketoconazole] 1% in the treatment of severe dandruff and scalp seborrhoeic dermatitis”

So, in summary: yes, there is evidence to suggest that when it comes to improving pattern hair loss, 2% ketoconazole is more effective over a six-month period versus 1% ketoconazole. The one percentage point difference does matter.

The questions then becomes: why?

Why is 2% ketoconazole better than 1% ketoconazole?

Ketoconazole is suspected to work in three ways to slow/stop hair loss and promote hair regrowth. The drug:

1. Reduces inflammation related to microbial activity on the scalp.
2. Reduces levels of dihydrotestosterone, the most powerful male hormone and the culprit behind AGA.
3. Prolongs the anagen phase (i.e., growing phase) of the hair cycle, thereby reducing excessive shedding.

We don’t exactly know why 2% ketoconazole is better than 1% ketoconazole. But, chances are that the 2% dilution simply accomplishes these things more effectively and (maybe) more rapidly, meaning that it:

1. Kills off more Malassezia, resulting in a more dramatic reduction in inflammation.
2. Reduces scalp DHT more effectively and more rapidly, preventing further follicle miniaturization in AGA.
3. Stimulates the transition to the anagen phase faster, thereby halting shedding and promoting hair regrowth in a shorter amount of time.

But with increasing efficacy, drugs often come with an increased risk of side effects. This is why clinical researchers often test several dilutions and doses of any drug: they’re trying to uncover which dilution or dose maximizes clinical efficacy while minimizing the risk of side effects.

So, with 1% versus 2% ketoconazole, does the increased concentration lead to an increased risk of side effects?

Does a 2% ketoconazole have a higher risk of side effects compared to 1% ketoconazole?

Although oral ketoconazole comes with significant side effects, these same side effects haven’t been reported with topical ketoconazole or ketoconazole shampoos.

This is because topical and shampoo formulations of ketoconazole are metabolized rapidly within the skin tissues, so very little (if any) topical ketoconazole actually reaches the bloodstream.

On that note, research continues to demonstrate that for the overwhelming majority of people, both 1% and 2% topical ketoconazole concentrations do not come with a notable risk of side effects.

Some individuals may experience a hypersensitivity reaction to ketoconazole topicals, however, this is relatively rare.

That being said, there is a small risk associated with the formulation of a 2% ketoconazole topical cream containing sodium sulfite. But this is a risk with the sodium sulfite, not the ketoconazole itself. And to be clear: sodium sulfite is not a standard ingredient in ketoconazole shampoo formulations (which are the ones prescribed for hair loss); it’s typically only found in topical formulations used to treat conditions like acne.

The bottom line: ketoconazole is rapidly metabolized in the skin, and therefore has minimal risks of side effects. This is why its 1% shampoo formulations are sold over-the-counter.

Should you use a 2% ketoconazole shampoo or topical?

Much like comparative studies between 1% and 2% ketoconazole, no studies have been conducted to assess whether a shampoo or a leave-on topical is more effective for hair growth.

But for now, the 2% shampoo formulation is probably the best way to go, and for two reasons:

1. Topical ketoconazole hasn’t been studied for hair loss
2. Topical ketocoanzole is not easy to find

In other words, 2% ketoconazole shampoo has several clinical studies demonstrating its efficacy, whereas topical ketconazole has only been evaluated in very small clinical studies (i.e.,  6 participants), and typically for conditions like acne (not hair loss).

Moreover, 2% ketoconazole shampoo is readily available – all you need is a prescription from your doctor. Topical ketoconazole is typically only sold for research purposes. And while topical ketoconazole would remain on the skin for longer (and thereby potentially have a greater effect on the hair follicles), we don’t think the potential additional benefits of topical ketoconazole outweigh the risks associated with acquiring and using it.

And with 2% ketoconazole shampoo consistently demonstrating a significant benefit for AGA sufferers, it makes the most sense to opt for what we already know is safe and works.

2% ketoconazole shampoo: clinical efficacy for pattern hair loss

• This study demonstrated that a 2% ketoconazole shampoo improves hair counts in men with AGA. It also found that 2% ketoconazole is nearly twice as effective as minoxidil.
• This study compared a few singular and combination therapies: minoxidil alone, finasteride alone, minoxidil + finasteride, and 2% ketoconazole shampoo + finasteride. Although the minoxidil + finasteride combination outperformed the ketoconazole + finasteride combination, it demonstrates that 2% ketoconazole can enhance finasteride’s benefits.
• This study found that 2% ketoconazole shampoo works well in combination with finasteride in minoxidil. Participants experienced hair regrowth in as little as 30 days.

The verdict: opt for a 2% ketoconazole shampoo

The available evidence suggests that when it comes to treating pattern hair loss (AGA), a 2% ketoconazole shampoo produces better, more rapid results than a 1% ketoconazole shampoo.

Yes, you’ll need to get a prescription for 2% ketoconazole. Yes, this requires an appointment with a doctor. And yes, this is a hassle. But in all likelihood, the benefits of 2% ketoconazole outweigh the convenience of the 1% formulation.

Questions? Comments? Please reach out in the comments section.