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Does a tight scalp cause pattern hair loss? This question recently resurfaced in hair loss forums… sparking heated debate from scalp tension supporters and opposers.

The supporters: scalp tension must contribute to hair loss. Why? Because balding men and women tend to have chronically tight scalps. This tension tends to match the pattern and progression of hair loss. And when we look at the effects of chronic tension in other tissues, we see near-perfect overlap with the biomarkers of a balding scalp: increased androgen activity, excess collagen deposition, tissue degradation, and hair loss.

Thus, scalp tension must be involved in pattern hair loss. Scalp tightness not only fits within the current androgenic theory, but also helps to answer many questions that the androgenic theory can’t – like why dihydrotestosterone (or DHT) increases in balding scalps… why DHT leads to hair loss in the scalp but hair growth in the chest and face… and why androgenic alopecia occurs in a specific pattern and progression.

But there’s one thing scalp tension advocates can’t explain: hair transplantation results. In fact, hair transplantation studies are the strongest opposition against the scalp tension theory. They’re also the rallying cry for the theory’s opposition.

The opposers: the entire idea that scalp tension contributes to pattern hair loss hangs on one major assumption: that our scalp environment influences our hair follicles’ ability to grow hair. However, this assumption is false. It was disproven in 1959 with the first study on hair transplantations. This study showed that…

1. Non-balding hairs transplanted to balding regions will keep growing normally.
2. Thinning hairs transplanted to non-thinning regions will keep balding at the same rate as other balding hairs in the scalp.

These findings, according to critics, demonstrate that androgenic alopecia has nothing to do with our scalp environment (or scalp tightness). Rather, pattern baldness must be genetically programmed within the follicles themselves. In other words, it’s the interaction between androgens and genetics that likely determines our hair follicles’ predisposition for hair loss and our baldness “clock”… not scalp tension.

So who is right? Who is wrong? And do these hair transplantation studies overturn the scalp tension-hair loss hypothesis… or are we missing something in our logic?

That’s what this article is for.

This is part two of a three-part series on scalp tightness and androgenic alopecia.

In the first article, we explored the science behind how scalp tension might contribute to androgenic alopecia. Now it’s time to build the scalp tightness counterargument.

First, we’ll dive into the scalp tension theory’s opposition and uncover the hair transplantation studies that changed the trajectory of hair loss research. Then we’ll reevaluate those studies in light of new evidence… and see if the conclusions from 1959 still hold today.

Finally, we’ll present new evidence to suggest that our scalp’s environment might influence our hair follicle’s ability to grow. In doing so, we’ll revisit the concept of donor dominance… and list some discrepancies in its theory.

By the end, we should have a firm understanding of the arguments for and against the scalp tension theory of androgenic alopecia. That way, you can decide what to believe. After all, hair loss research is always up for reinterpretation.

If you have any questions, I’m happy to address them in the comments.

The argument against the scalp tension theory: hair transplantation studies

In 1950, the scalp tension theory of androgenic alopecia had picked up steam in scholarly journals. But it wasn’t until 1959 that researchers figured out how to test its plausibility.

That year, a researcher named Dr. Orentreich set up an experiment to understand which factors influence why we go bald. His major question: is baldness due to a hair follicle’s environment (i.e., its surrounding tissue)… or is it due to the hair follicle itself?

Dr. Orentreich thought of an ingenious way to test this. Hair transplantations. Specifically, he wanted to see if a balding hair transplanted out of a balding scalp would continue to bald… and if a healthy hair transplanted into a balding scalp would continue balding. He figured that if balding had anything to do with our scalp environment, healthy hairs moved to balding regions would start to bald – and balding hairs moved to healthy regions would stop balding.

So he gathered patients with androgenic alopecia (AGA) and performed his tests:

1. He took skin grafts (6-12mm punch biopsies) of balding scalp regions and transplanted those grafts into non-balding parts of the scalp.
2. He took 6-12mm punch biopsies of non-thinning scalp regions and transplanted those biopsies in balding parts of the scalp.

So, he got busy observing (and waiting). Years later, he published his findings. What were the results?

Balding hairs keep balding, and non-balding hairs keep growing… no matter where we put them

That’s right. After 2.5 years of observation, Oreintreich found that…

• Non-balding hairs transplanted to balding regions will keep growing normally.
• Balding hairs transplanted to non-thinning regions will keep thinning at the same rate as balding hair at the top of the scalp.

Thus, he concluded that our scalp environment had no influence over a hair follicle’s determination to start thinning. To quote directly from his study…

“…The determinants of growth of strong scalp hair or of baldness lie within the local skin tissues of a full-thickness graft and suggest that the pathogenesis of common male baldness is inherent in each individual hair follicle. Probably each individual follicle is genetically predisposed to respond or not to respond to androgenic and/or other influences that inhibit its growth”

Dr. Orentreich referred to scalp hair follicles as donor dominant – meaning that scalp hairs retain all of their characteristics regardless of where they’re placed. In his words…

“…The transposed grafted skin maintains its integrity and characteristics independent of the recipient site.”

These findings undermined the scalp tension hypothesis entirely. But this was just one study. In order to be sure, we’d need to see these results occur again… and again.

Over the next two decades, that’s exactly what happened.

Follow-up studies confirm Dr. Orentreich’s hair transplantation findings

In 1979, a researcher took composite skin grafts of balding, non-balding, and bald scalp regions from a 29-year old patient, then transplanted those skin grafts to the forearm and observed their hair growth over the next several months.

His findings? When those scalp skin grafts were moved to the forearm, bald hairs stayed bald, thinning hairs continued to thin, and non-thinning hairs remained thick and healthy.

Then in 1982, doctors from the Oregon Regional Primate Center used a similar skin graft procedure to transplant the hairs of balding primates from the backs of their scalp (i.e., where hair was healthy) to the front of the scalp (i.e. where these stump-tailed macaques were experiencing human-like pattern hair loss).

Eight years later, the primates’ donor hairs were still alive – despite the fact that their surrounding follicles had succumbed to baldness. Again – the evidence confirms that transplanted hairs don’t miniaturize – and that hair follicles aren’t affected by their environment.

So… is the scalp tension theory officially debunked?

Well, let’s review the evidence:

• Early hair transplantation studies show that transplanted hairs don’t miniaturize… even when they’re transplanted into “tense” (i.e., balding) scalps
• Some of those studies show that balding hairs keep miniaturizing… even when they’re removed from a balding environment and placed on the forearm.

Based on these findings, it’s completely rational to assume that the scalp tension theory is invalid. In other words, our scalp environment does not influence a hair follicle’s growth. Hair transplantation studies confirm this belief. And as such, the scalp tightness theory is debunked. Right?

Well, not so fast.

We’ve really only built a straw-man’s argument against the scalp tightness-pattern hair loss hypothesis. Why? Because we’ve yet to address the two elephants in the room.

Elephant #1: relieving scalp tension improves AGA outcomes

There’s evidence that relieving scalp tension – either through mechanical offloading or Botox injections into “tight” scalp muscles – improves hair counts in AGA sufferers… and on-par with the effectiveness of finasteride. We discussed these findings in our original scalp tension article.

So if scalp tension doesn’t contribute to AGA… for some reason, relieving scalp tension helps reverse it. Go figure.

Elephant #2: hair transplant studies don’t answer every question needed to refute the scalp tension-AGA hypothesis

Let’s look at these studies’ conclusions again. What are they saying?

If we take a chunk of skin from the back of our heads and insert it into a balding region, that skin’s hair will continue to grow for several years.

But if we’re to refute the scalp tension hypothesis, that’s not what we should be testing.

This is because we haven’t yet isolated the variable to which we’re making inferences… the actual hair follicle.

Rather, these studies evaluate how entire landscapes of skin behave when moved to different locations of the body. Accordingly, here’s how the conclusions of those studies should’ve read:

When harvesting 6-12mm skin punch biopsies, the 20-80 hair follicles within those biopsies retain their growth characteristics regardless of where they are transplanted on the scalp, even in men with AGA.

Now, what does this conclusion not tell us?

1. If a hair follicle’s immediate environment (i.e., its skin tissues and surrounding hair follicles) influence its growth characteristics.
2. If older hair transplants “strip” techniques achieve the same lasting results as individual hair follicle transplants
3. If transplanted skin experiences the same tensile environment as surrounding skin

Again, these hair transplantations are incredibly important. But they don’t answer these questions. And if we’re to refute the scalp tension hypothesis, we need to evaluate each of these questions carefully.

That’s what the rest of this article is going to do. And in doing so, we’ll see issues in using early hair transplant studies as evidence against the scalp tightness theory.

1. Does a scalp hair follicle’s surrounding environment influence its growth characteristics?

Contrary to what those initial hair transplant studies suggest, a hair follicle’s environment does influence its behavior. We’ve seen this demonstrated in three major ways:

• Scalp hairs change growth behaviors depending on where they’re transplanted
• Balding human hair, when transplanted on mice, can regenerate in one hair cycle
• Hair follicles directly next to each other can coordinate / hair growth

Let’s take these one-by-one.

Scalp hairs change growth rates depending on where we transplant them

In 2002, a team of researchers published a study that revised aspects of Orentreich’s “donor dominance”. The team’s first research question: over a three-year period, what happens if we transplant scalp hairs from the back of our heads to our lower leg?

The results: 60% of transplanted hairs survive, and the ones that survive grow at about half the speed of regular scalp hairs.

Their second research question: what happens if we re-harvest those scalp-hairs-turned-leg-hairs and move them back to the scalp (or more specifically, the nape of the neck?)

The results: those re-transplanted hairs – which were once scalp hairs, then leg hairs, and now are neck hairs  – grow at a slower speed than non-transplanted scalp hairs. However, they grow at the same speed of hairs transplanted directly from the scalp into the neck.

The takeaways: scalp hair follicles adapt to growth rates set by their surrounding environment. Thus, scalp hair follicles can be influenced by the location in which they are transplanted.

Moreover, a follow-up study showed that chest hairs, when transplanted into balding scalps, grow longer to match the length of surrounding (but still balding) scalp hairs.

Together, these findings suggest that scalp hair follicles are not 100% donor dominant… and that scalp environment can influence the behavior of its recipient hairs.

As for why? The investigators weren’t sure. But they hypothesized this could be due to “recipient site characteristics such as vascularity, dermal thickness or skin tension.”

Again — that’s not to say that donor dominance is invalid — or that scalp hairs transplanted into balding regions won’t grow. We’re just highlighting that recipient sites of scalp hairs can influence that hair’s growth characteristics — which goes against the idea that scalp hairs are 100% donor dominant.

This begs the question… just how much influence can a recipient site have on a hair?

Apparently a lot. And here is where things get more interesting.

Balding human hairs can regenerate when transplanted onto a mouse

A 2002 study from the Orentreich Foundation for the Advancement of Science (yes, the very same Dr. Orentreich) transplanted both balding and non-balding human hairs into the backs of mice. 22 weeks later, what were the findings?

The balding human hairs had regenerated just as well as the healthy non-balding hairs… and this regeneration happened in a single hair cycle.

In fact, those balding hairs continued thickening through the duration of the study… whereas the non-balding hairs, for reasons unknown, plateaued after 17 weeks.

How is that possible? Aren’t balding human scalp hairs supposed to continue to thin – like they did in that case study of the 29-year old whose balding scalp hairs were transplanted to his forearm?

Again, the researchers couldn’t explain their results with 100% certainty. They thought the regeneration might be due to lower androgen levels in mice – similar to how finasteride (an androgen reducer) might improve hair loss in men. But the hairs regrew just as well on male (higher androgen) and female (lower androgen) mice — which they couldn’t explain.

Even odder – the balding hairs regenerated in a single hair cycle – much faster than hair recoveries seen from finasteride in humans. To the researchers, this suggested the influence of non-androgenic factors in the recovery of those hairs. Yet that was as far as they could extrapolate.

Again, this contradicts the original hair transplant studies. Balding hair follicles should keep thinning no matter where they’re placed. Except this study shows that’s not always true.

So, are there any other examples of hair follicle regeneration from environmental influence?

Yes. And this next study even gives us insights as to what may explain the discrepancy in newer findings versus the original hair transplantation studies.

Hair-plucking increases hair follicle proliferation five-fold… but only if many hairs are plucked from a small region

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 its normal pre-plucking density. 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.

What does this show? Two things…

1. A hair follicle’s immediate environment can influence its ability to grow. We saw this in changing the hair’s environment (i.e., transplanting balding human hair onto a mouse)… and by augmenting that environment (i.e. plucking many hairs from a small region). In both cases, hair recovery ensued.
2. The immediate environment that hair follicles use to cross-communicate can be very small.

Let’s elaborate on that second point. For reference, those plucking “zones” the investigators used ranged from 2.4mm to 8mm – yet researchers only observed hair follicle proliferation in plucking zones of 4mm and smaller.

Now let’s reflect back to those original hair transplantation studies.

These studies used skin punch biopsies of 6mm to 12mm – each of which contained up to several dozen hair follicles. Yet our inferences from those transplantation studies were that scalp hair follicles are donor dominant – they retain their characteristics wherever they are transplanted.

Do you see the irony?

We’re saying that hair follicles can coordinate to make new hair follicles across distances of 4mm distances or smaller… while simultaneously saying that scalp hair follicles aren’t influenced by the environment, as demonstrated by transplanting 6-12mm chunks of skin containing dozens of hairs and watching them not change their behavior.

So… does the amount of tissue transferred alongside hair follicles influence hair transplant results?

This is actually the second question we need to answer in order to refute the scalp tension hypothesis. And while nobody’s actually fully answered this question… preliminary evidence suggests that yes -the amount of tissue transferred alongside a hair follicle transplant does influence its survival.

2. Does the success rate of a hair transplant depend on how much adjacent tissue is transferred alongside the hair follicles?

In both Orentreich’s original study and the primate transplant study, hairs from skin punch biopsies of 6-12mm retained their original characteristics when transplanted into balding regions – and for 2.5 to 8 years.

But again, these punch biopsies contained dozens of hair follicles and their surrounding tissue. As we’ve just learned, surrounding hair follicles and tissues communicate with each other to react to environmental influences.

But do these tissues also help hair follicles maintain their original growth characteristics?

In other words, if we strip away these tissues, isolate a hair follicle unit to just a single hair follicle, and then transplant that into a balding region, what happens?

Interestingly, those hair follicles don’t always survive.

Hair follicle transplant survival rates decrease if individual hairs – rather than full hair follicle units – are transplanted

This is exactly what these researchers discovered when investigating hair transplant survival rates for individual hairs versus hair follicle “clusters” – known as hair follicle units.

Specifically, these researchers were exploring a new hair transplantation technique known as follicular unit extracts (or FUE). This is when, rather than taking larger punch biopsies or “strips” of skin containing hundreds of hair follicles – a surgeon instead takes a series of 0.6-1.2mm “punches” containing individual hair follicle units (usually 4-8 hairs) spread throughout the donor area. This allows for less scarring from a transplant.

Their findings: if a hair follicle is separated from its follicular “unit” – its survival rate decreases. In fact, single hair follicles are 25% more likely not to survive… at least in the 26-week period of the study.

In the words of the study:

“Extremely high survival rates of micrografts are obtainable by transplanting intact follicular clumps with protective tissue around the micrograft, and preserving the follicular clump’s sebaceous gland. These survival rates were not achieved when micrografts were produced by splitting individual hairs away from a naturally occurring follicular clump.”

Do hair transplantations always last forever?

With 6-12 punch biopsies and “strip” transplantations, these hairs certainly last for a very long time. Certainly long enough to validate the surgery (if you’re considering doing it).

But as with these techniques – and with newer techniques, like follicular unit extractions (FUE) – survival rates seem to depend on how much connective tissue is also transplanted alongside the hair follicle, and if a hair follicle unit is transferred altogether.

I haven’t found any studies investigating the long-term efficacy of FUE transplantations. But it seems like there’s enough preliminary evidence to suggest that the less surrounding tissue transplanted alongside the hair, the less successful the hair transplant.

In FUE literature reviews, researchers address these concerns by acknowledging that, over time, even donor regions of a scalp can still succumb to miniaturization from pattern hair loss. In other words, over the years, the loss of transplanted hairs is perhaps to be expected.

“While the follicular units in the optimal donor area of the occipital and parietal scalp are ″relatively″ protected from androgenetic hair loss, even those follicular units may be somewhat affected with time.”

For the record, this is absolutely true. In many cases of androgenic alopecia, regions beyond the galea aponeurotica will succumb to hair follicle miniaturization – especially in advanced stages. And the truth is that regardless of an FUT or FUE procedure, hair follicle survivability is likely dependent, in part, on how much tissue the surgeon trims away from each follicle prior to transplanting it.

Additionally, as more surgeons transition to FUE, many now mandate to their patients to take finasteride. In fact, a lot of surgeons won’t even perform FUE surgery unless their patient agrees to this.

Obviously, this is to the interest of the patient. Finasteride is incredibly powerful at stopping hair loss – and as more FUE patients commit to taking it, it will improve their odds of their hair transplant sticking and looking great for years to come.

At the same time, mandating finasteride use post-FUE transplantations will make it harder to grasp how individually transplanted hair follicle units (and sometimes, just single hair follicles) behave over decades in a balding environment. The FUE studies bank on these follicles behaving the same way as they did in the original hair transplantation studies. But again, I’m not sure this is the case.

Perhaps unsurprisingly, a lot of readers here who did an FUE and then stopped taking finasteride have reported that their transplanted hairs are falling out. That’s concerning – especially as these readers have also reported that the regions from where those transplanted hairs were taken have not had any noticeable miniaturization.

While many surgeons claim this only happens if a transplanted hair is taken too close to the vertex (where thinning might later occur) – this seems to happen far too often to explain all cases.

Again, here’s a 2013 literature review suggesting these newer, smaller “micrograft” techniques might not match up to Orentreich’s hair transplant findings with larger punch biopsies…

“Micrograft survival rates in hair transplantation have been frequently described in private conversations by hair transplant doctors as variable at best. References in medical literature may grossly underestimate the prevalence and magnitude of poor growth. This is probably because most hair transplant surgeons are concerned that publication of a significant incidence of poor growth would reflect negatively on their practice.”

In my conversations with other AGA researchers, a few have stated – contrary to popular belief – that transplanted hairs do thin. There’s even a hypothesis that transplanted hairs simply restart their “balding clock” post-transplantation – meaning that in 5, 15, or 25 years, we can expect transplants to start thinning as well.

Only time will tell.

In any case, there at least appears preliminary evidence that a hair follicle’s surrounding environment influences its growth characteristics… that this includes both balding and non-balding scalp hairs… and that hair transplantation success might depend on how much of the surrounding environment is transplanted along with the hair.

Do transplanted hairs experience the same “tensile” environment as recipient site hairs?

Another thing we’d need to confirm for hair transplantations to refute the scalp tension hypothesis is that after an operation, transplanted hairs experience the same tension as the recipient site hairs.

Unfortunately, this hasn’t yet been studied. But based on what has been studied, we can infer that this might or might not be the case.

Interestingly, in that eight-year transplant study on balding primates, investigators biopsied the transplanted skin periodically after the procedure – to see what was going on underneath the skin.

They found that after one week, transplanted tissues fused with surrounding tissues. Soon after, the transplanted hairs fell out, and then began regrowing a number of weeks later as underlying tissue began to merge toward the transplanted tissue. At four months, the underlying transplant tissue looked nearly identical to the surrounding tissues – minus the larger hairs.

This might suggest that these hairs do experience the same tension as surrounding hairs, but it’s really hard to say. What isn’t studied here is the differences in tensile readouts between transplanted hair follicles and their surrounding environments. As another researcher mentioned in his critique of the balding scalp hair-to-forearm transplant study we mentioned earlier…

“…According to the approach of the present paper, it would be necessary to know the strain supported by the forearm skin and to realize that the hair follicles close to receding hairline have already started a countdown toward the miniaturization, but not the occipital follicles. In hair transplantation, the grafted follicles start a new “balding clock,” but hair growth would be guaranteed for many years even without preventive pharmacotherapy.”

What also isn’t studied is the role of epigenetics in these transplants – or in other words, the changes in gene expression pre- and post- hair transplantation. When these transplant studies were conducted, epigenetics wasn’t even a field of scientific study. So again, there are just a lot of unknowns here… so we need to exercise caution with how we interpret these studies and apply implications.

In any case, we can now summarize why hair transplantation successes might not refute the scalp tension-AGA hypothesis.

Summary: why hair transplants might not refute the scalp tension-hair loss theory

Hair transplantations are overwhelmingly successful. Early transplant studies suggested that scalp hairs transplanted into balding scalp environments retain their original characteristics and keep growing forever – a concept known as donor dominance. Many people use these studies to refute the scalp tension hypothesis – and with good reason.

At the same time, relieving scalp tension appears to improve androgenic alopecia (for references, please see the first article). So we should probably try to make sense of these paradoxical findings.

Reevaluating the original hair transplantation studies, we see that the investigators transplanted 6-12mm skin punch biopsies containing dozens of hair follicles per transplant. This might create a few problems when trying to use these studies as evidence against the scalp tightness-AGA theory:

• Studies show hair follicles communicate with each other to maintain or increase hair follicle counts in regions of 4mm and smaller. Thus, we can’t conclude that baldness is determined within each hair follicle if these transplant studies use punch biopsies large enough to allow for inter-follicular communication.
• There’s preliminary evidence that as we trim away surrounding tissues, hair follicle transplantation survival rates decrease. This is most obvious in FUE micrograft studies of single hair follicles – where researchers separate a hair follicle from its hair follicle unit, and then observe worse survival rates post-transplantation into balding regions.
• Moreover, recent studies demonstrate that human scalp hair follicles do take on characteristics of their recipient sites… and that balding human hairs can regenerate in a single hair cycle if transplanted onto the back of a mouse. In other words, human scalp hairs are susceptible to their environment – which refutes aspects of Orentreich’s original findings.

These findings, along with many anecdotes from patients with failed FUT and FUE transplants (despite no miniaturization observed from where the hairs were transplanted), have led some AGA researchers to conclude transplanted hair follicles might eventually thin. Rather, it’s just that after transplantation, their “balding clocks” are set back to zero… and thus we might need to wait 5, 15, or 25 years to begin to see the effects.

Again, this is not to say hair transplants aren’t long-lasting. In most cases, they certainly are. It’s just to say that there’s evidence that transplanted hairs might also be susceptible to AGA with time… and that recipient sites of transplanted balding scalps have a bigger influence on their growth than we initially thought.

How can transplanted hairs grow in fibrotic scalp environments?

According to some models of the scalp tension hypothesis, fibrosis (or scar tissue) is a rate-limiting factor for hair recovery. This has led some to ask, “If regular hair can’t grow in fibrotic tissues, how come transplanted hairs can?”

Interestingly, we can use the findings of a recent (and fascinating) study to help answer this question. It was conducted, in part, by one of the biggest names in hair loss research: Dr. George Cotsarelis.

Dr. Cotsarelis and his team wanted to understand the role of the hair follicle during wound-healing. It has been long understood that where there is scar tissue, hair cannot grow. We see this in burns, scleroderma patients, and in advanced stages of androgenic alopecia (pattern hair loss) where scar tissue is present in skin tissues, thus preventing the proliferation of hair follicles (and thereby hair growth).

What Cotsarelis and his researchers discovered: if we can regenerate a hair follicle first, that hair follicle will begin to signal to its surrounding tissues to regenerate other cell types normally lost to scar tissue – like adipose tissue (or subcutaneous fat).

What does this have to do with hair transplant survival rates? Well, think about it:

• In AGA, fibrosis (scar tissues) restricts hair follicle growth space, leading to hair loss.
• Hair transplants take hair follicle units from the backs of our scalps and transplant them into balding areas where there is scar tissues
• In doing so, they provide scarred tissues with newer, healthy hair – and in a way, “force” the regeneration process of nearby tissue – thus partially resolving fibrosis in surrounding tissues and allowing for the transplanted hairs to grow.

Interestingly, this might be why some hair transplant surgeries observe transplant survival rates of over 100%. This was originally believed to be the result of hidden telogen (resting) hairs moved during the hair transplant. Now it’s possible that these extra hairs are actually bald vellus hairs regenerating as a result of cellular signaling from the transplanted hairs.

In fact, this study might not only explain why transplanted scalp hairs survive in balding environments… but also the mechanisms behind why they reset the baldness clock – if we choose to believe that concept at all.

Final remarks: scalp tension and hair transplants

The scalp tension-AGA hypothesis is far from proven, but it’s also far from debunked.

At face-value, older hair transplantation studies refuted the scalp tension theory and led researchers to believe that hair follicle miniaturization was programmed within the hair follicle itself – not its environment.

However, these transplant studies were conducted using 6-12mm skin punch biopsies. A 6-12mm biopsy contains dozens of hair follicles and a lot of surrounding tissues. That’s a far cry from a single hair follicle. Resultantly, 6-12mm punch biopsies don’t really tell us much about what happens if we transplant an individual hair follicle into a balding region – absent of its surrounding tissues.

New research suggests that surrounding tissues do influence the regulation and proliferation of the hair follicles they support. And interestingly, survival rates for transplanted hairs decrease as we trim away surrounding tissues and transplant just singular instead of entire hair follicle units (4-8 hairs), strips, or punch biopsies.

This suggests the conclusions of the hair transplant studies from 1959-1982 actually should attribute more of their success to the surrounding tissues transplanted alongside the hair follicle – and the fact that entire hair follicle units were transferred (not just single hairs) – which likely allowed these tissues to maintain follicular communication and regular their growth and proliferation even in their newly transplanted environment.

Given all of this, and the potential variability in success with FUE transplants, several AGA researchers now believe that transplanted hairs simply reset on a balding clock – and that given enough time, they eventually will thin.

On top of that, newer studies show that healthy transplanted hair follicles actually help to signal to surrounding tissues to regenerate – just explaining why they can proliferate in balding regions (or maybe even support the proliferation of surrounding balding hairs).

All of this isn’t to say that the scalp tension hypothesis is irrefutable. On a personal level, I don’t think that scalp tension explains all aspects of AGA (more on this later). This is just to say that hair transplantation studies don’t necessarily refute the scalp tightness theory – especially in light of newer evidence.

At the end of the day, relieving scalp tension – either through botulinum toxin injections or mechanical offloading – seems to improve AGA outcomes. So if scalp tension doesn’t contribute to pattern hair loss… relieving scalp tension seems to still help regrow hair.

Is the scalp tension theory true? I don’t know. Maybe. Maybe not. But I don’t think these original hair transplant studies refute it. And in the next article, we’ll discuss where this “scalp tension” might originate.

In 2016, an Italian surgeon made hair loss headlines after announcing the accidental discovery of a topical formula that showed promise in slowing, stopping, and even reversing hair loss. Its name? Brotzu Lotion — titled after the creator himself: then-81-year old Giovanni Brotzu.

What happened next is what always happens: hair loss forums went wild.

Hair loss sufferers began researching the ingredients in Brotzu Lotion’s patent. They organized group buys to source, compound, and self-distribute crude versions of the lotion ahead of Brotzu’s expected 2018 release.

Some hair loss sufferers even contacted Dr. Brotzu himself — who, in correspondence, suggested that the lotion could turn back the balding clock by 5 years… and that there are no reported side effects.

Nearly two years later, where do we stand?

Since then, excitement for Brotzu Lotion has fizzled, returned, died, and just recently… exploded. The question is: will Brotzu Lotion — set for a 2018 release in Europe — actually live up to the hype?

I’m cautiously optimistic, with caveats. Emphasis on caution and caveats. This article explains why.

We’ll uncover the science behind Brotzu Lotion — its ingredients, mechanisms of action, and 120-day study results. Then we’ll dive into Brotzu’s before-after hair regrowth photos — along with some photos people claim are from Brotzu Lotion, but really aren’t.

Finally, we’ll reveal which kinds of hair loss the lotion may help — pattern hair loss (androgenic alopecia) or autoimmune-related hair loss (alopecia areata and alopecia universalis) — and if you’re planning on trying Brotzu Lotion, where to set your hair regrowth expectations.

Brotzu Lotion: A Hair Loss Breakthrough… Or All Hype?

Brotzu Lotion is a topically-applied hair loss lotion expected to arrive in Europe in late-2018.

At first glance, this is no big deal. After all, there are dozens of lotions used to combat hair loss — from FDA-approved drugs like minoxidil (Rogaine) to less conventional topicals like emu oil, rosemary oil, or even topical finasteride (Propecia). So what makes Brotzu Lotion worth any attention?

Three things.

Firstly, its inventor claims that for most users, Brotzu should reverse balding by five years within 18 months of use. That’s a huge claim in the hair loss world — one not even Propecia makes.

Secondly, a few great before-after hair regrowth photos are already circulating online — spurring excitement for many hair loss sufferers.

Thirdly, its ingredients and the way the lotion works (its mechanisms of action) are novel — meaning we’ve yet to see a topical target hair loss this way before (at least one that’s made it to market).

Let’s take these one-by-one.

Who Is Giovanni Brotzu — The Inventor Of Brotzu Lotion?

Whenever we hear of a new hair loss treatment, we should look at the person behind the discovery. Are they reputable? Are they operating under a pseudonym? Are they actually just a marketer? Or are they a scientist, working alongside a research team, with published literature to back up their claims?

Oftentimes, this all we need to determine if a new hair loss “breakthrough” is all-hype or the real deal. And encouragingly, in this case, Brotzu Lotion’s inventor (Giovanni Brotzu) is no quack.

Dr. Brotzu is a retired vascular surgeon. He’s the holder of several provisional patents for surgical implants, and his late father — a pharmacologist — was once a candidate for the Nobel Prize.

So how does one go from vascular surgeon to hair loss lotion creator? According to Brotzu, by accident.

Dr. Brotzu’s team was trialing a drug to treat a complication of diabetes: vascular insufficiency in the legs (which can lead to limb loss). When they saw the drug improved vascularity and hair growth on subjects’ legs, they reformulated it into a topical — and tested it on a nurse with hair loss on her scalp.

The results were impressive enough for Dr. Brotzu to pilot more case studies and then create a patent around the formula… which grabbed the attention of the Fidia Pharma Group — a pharmaceutical company. That’s when Brotzu Lotion picked up attention on hair loss forums… and when people started asking for photo evidence.

They didn’t have to wait long. Within the year, photos started circulating — along with study results.

Brotzu Lotion — Early Results (Hair Regrowth Photos)

So far, Brotzu Lotion has been studied on two types of hair loss: autoimmune hair loss (like alopecia areata and alopecia universalis) and pattern hair loss (also known as androgenic alopecia).

Results: Brotzu Lotion For Autoimmune Hair Loss (Case Studies)

Initial case studies (i.e., single-person tests) with Brotzu Lotion show promise for an autoimmune condition called alopecia areatea. This is when a person loses hair, usually in patches, anywhere on the scalp (the sides, tops, and backs of the head — and even the eyebrows). In advanced stages, this leads to hair loss everywhere on the body (alopecia universalis).

In a 2016 presentation, Dr. Brotzu showcased Brotzu Lotion’s one-year hair regrowth results for a female child suffering from alopecia universalis. Here are her before-after photos:

That’s significant hair recovery — and for those with alopecia areata / universalis — incredible results.

Encouragingly, Dr. Brotzu’s patent cites more case studies (but no photos) and claims improvement for pretty much all of his subjects with autoimmune-related hair loss. In fact, he even presented more before-after photos of autoimmune hair loss subjects (here’s the link  — start at 10:30) at another conference. The takeaway? Similar results. See this screenshot:

Another near-full recovery from alopecia areata — and in 16 months.

What’s yet-to-be determined: how much hair regrowth alopecia areata / universalis sufferers can expect. So far, it looks like full recoveries are within the realm of possibilities.

But is the same true for pattern hair loss — a much more common type of hair loss? Can androgenic alopecia sufferers expect similar recoveries — or even to shave five years off the “balding clock”?

Unfortunately — at least so far — the data suggests probably not.

Brotzu Lotion For Pattern Hair Loss (A Clinical Study)

In April 2018, Dr. Brotzu presented preliminary study results of Brotzu Lotion for pattern hair loss.

As with any study, its design matters. So here’s a quick overview of the study design…

• Subjects: 30 males, 30 females — all with androgenic alopecia
• Treatment: 1mg of Brotzu Lotion, applied daily in balding regions
• Duration: six months — with follow-ups at months 0, 1, 3, and 6

…And here’s what the team measured at each follow-up session:

1. Scalp exam — to check for skin quality changes (i.e., side effects)
2. Hair diameter — a surrogate for hair thickness
3. Photographic analysis — to measure the total number of hairs, the percent of anagen hairs (hairs in their growth phase), and the percent of telogen hairs (hairs in their resting phase)

(Note: the investigators also measured hair fall during wash tests and tug tests. But for androgenic alopecia — these metrics are basically useless, so we won’t cover them).

Brotzu Lotion’s Six-Month Results For Androgenic Alopecia (And Photos)

After six months, here were the study’s findings:

• Scalp exam — no changes (no side effects)
• Hair diameter — no significant changes
• Photographic analysis — an increase in anagen hairs (growth phase), a decrease in telogen hairs (resting phase), and no mention of the overall change in hair count

The two major takeaways are that 1) hair thickness did not change, and 2) while the ratio of hairs in the growth vs. resting phase improved, we still don’t know about the overall change in hair count (unless I missed it somewhere — which is possible, since the presentation was in Italian).

So how do these results translate into photographs?

Here are two subjects Dr. Brotzu highlighted in his presentation. First, a before-after photo of a male:

Next, a before-after photo of a female:

The takeaways? Very little regrowth for the male, and maybe slightly more regrowth for the female — though it’s hard to say. It seems like the female got her roots colored between photos, and in the “after” photo, her dyed blonde hair may just blend better into the scalp skin.

What Should We Make Of Brotzu’s Results For Pattern Hair Loss?

I’m not impressed, but I’m also not surprised.

When it comes to pattern hair loss, it’s hard to find a good treatment. In fact, most topicals / supplements on-the-market for androgenic alopecia (pattern hair loss) are either completely ineffective, or only demonstrate hair regrowth on paper (in a study) — with any marginal changes in hair count rarely translating to photos.

Long-story short: the above results are, sadly, ones we’ve come to expect for pattern hair loss.

But how is that possible? After all, people suffering from autoimmune-related hair loss showed major hair recoveries using Brotzu Lotion. Why aren’t we seeing the same results for pattern hair loss?

Well, autoimmune hair loss is not pattern hair loss. They’re entirely different conditions. And unfortunately, hair loss forums confuse the two all the time.

Autoimmune Hair Loss Is Not Pattern Hair Loss

Autoimmune hair loss presents as patchy hair loss anywhere on the scalp. Pattern hair loss presents as a receding hairline, a bald spot, or general “diffuse” thinning above the sides of the scalp.

Autoimmune hair loss is when the body confuses its own hair follicles as foreign invaders. Pattern hair loss is the result of an interplay between genetics, hormones, and skin remodeling (fibrosis).

Autoimmune hair loss accounts for less than 5% of hair loss cases. But pattern hair loss? 95% of cases.

While both conditions are linked to inflammation, but only pattern hair loss leads to scarring. And while both conditions result in hair loss, their pathologies — and thereby treatments — vary wildly.

The bottom line: we should never assume treatments for alopecia areata will translate to androgenic alopecia (pattern hair loss). It’s making an apples-to-oranges comparison.

So… Should We Dismiss Brotzu Lotion For Pattern Hair Loss Entirely? No

Firstly, we need to keep in mind that hair loss treatments take a long time to work.

For reference, studies show that finasteride (Propecia) takes two years before reaching full efficacy. Minoxidil (Rogaine) takes 6-12 months. And Dr. Brotzu himself said that the lotion needs 18 months for the full effect.

Brotzu Lotion’s study was only six months long. Maybe a six-month study wasn’t long enough to see significant results. We won’t know until Fidia Pharma releases more data.

Secondly, the Brotzu family continues to release more androgenic alopecia before-after photos… and some of these photos do show significant hair recovery.

In fact, following backlash in one hair loss forum, Dr. Brotzu’s son registered a username (and chimed in) to defend his father’s lotion — and with a new case study. His response, translated: “Statistics are used in medical congresses, photos are used in advertising.”

He then shared photos of a better responder — a male using Brotzu Lotion for two months…

…and to me, these results are significant, and worth sharing. Which makes me wonder why Dr. Brotzu didn’t share more photos like this during his presentation.

Brotzu Lotion: Key Takeaways From Study Results (So Far)

In any case, we have enough information to draw a few conclusions:

1. Brotzu Lotion, on average, may work well for autoimmune-related hair loss
2. Brotzu Lotion, on average, may only marginally improve pattern hair loss in six months
3. Brotzu Lotion, for a small percentage of pattern hair loss sufferers, may work amazingly

And while I have reservations about Brotzu Lotion reversing our baldness “clock” by five years, I also find the lotion’s mechanisms of action to be novel, fascinating, and a step in the right direction for hair loss treatments.

In fact, the way the lotion works is almost like minoxidil (Rogaine) meets a topical finasteride (Propecia) — but through different mechanisms, and without the side effects (so far).

And to understand how, we need to understand Brotzu Lotion’s ingredients. [Note: the following section gets a bit technical, and if you’re not interested, there’s a summary of everything at the bottom of this article.]

Brotzu Lotion’s Ingredients

According to its patent, Brotzu Lotion primarily consists of three ingredients:

• Propionyl-L-Carnitine — an amino acid (protein)
• S-Equol — a non-steroidal estrogen derived from soy
• Dihomo-Gamma-Linoleic Acid (DGLA) — an omega six fatty acid

This is already a bit of a mouthful. So let’s break down each ingredient, rationalize why they’re included, and explain how all of them — when combined — may be synergistic for our hair.

How Brotzu Lotion’s Ingredients May Help Regrow Hair

Ingredient #1: Propionyl-L-Carnitine

When it comes to any hair loss topical — whether it’s minoxidil (Rogaine) or rosemary essential oil — penetration and metabolism of the “active ingredients” are key to a topical’s success.

For instance, if a hair loss topical ingredient helps regrow hair, but its ingredients can’t penetrate the top layer of our scalp skin, it’s useless. It won’t reach all the way down to our hair follicle dermal papilla cells — the place the ingredients must reach in order for the lotion to work.

And if that same ingredient penetrates our scalp skin, but it can’t be metabolized (absorbed) by our hair follicle cells, then it’s still useless. We need our scalp tissues to absorb (and use) those ingredients. Otherwise, they’ll just sit there indefinitely.

In the topical world, there’s a name for substances that help with penetration and/or metabolism: carriers. For example, minoxidil’s carrier (among many) is a substance known as propylene glycol. It helps minoxidil penetrate and absorb into the skin, which is why manufacturers add it to minoxidil to manufacture Rogaine.

Brotzu Lotion’s equivalent to a “carrier” is an ingredient called propionyl-l-carnitine.

Propionyl-l-carnitine is a protein. It’s also a derivative of l-carnitine. It’s associated with antioxidant activity  and, importantly, the improved transportation of fatty acids to cells…

…which is exactly why it’s used in Dr. Brotzu’s formula. Propionyl-l-carnitine increases the metabolism of a certain fatty acid ingredient (keep reading), and it also improves the metabolism of its two main ingredients.

So what are Brotzu Lotions main ingredients? A plant-derived compound that helps reduce DHT, and a fat-derived substance that improves blood flow: S-equol and dihomo-gamma-linoleic acid (DGLA).

Ingredient #2: S-Equol

S-equol is a compound derived from soy. It’s part of a class of chemicals called isoflavones. Specifically, it’s a phytochemical (a chemical from a plant). Even more specifically, it’s a phytoestrogen — a plant estrogen that looks structurally like human estrogen, but when we ingest it, it has a much weaker effect.

How Might S-Equol Improve Hair Growth? It Decreases Androgen Activity (DHT)

Research suggests that S-equol may help reduce a hormone known as dihydrotestosterone, or DHT.

Dihydrotestosterone (or DHT) is a hormone made from testosterone. It’s also suspected to play a major role in pattern hair loss. Why? Because 1) DHT is elevated in balding scalp tissues, and 2) men who can’t produce DHT (due to castration or a genetic deficiency) never go bald.

As a result, many hair loss treatments target to reduce scalp tissue DHT. And while DHT certainly isn’t the only factor in AGA, the evidence is clear: if we reduce DHT to castration levels (for example, with dutasteride), we can usually stop pattern hair loss progression for most men.

S-equol is one compound that may help reduce DHT levels, and thereby help fight hair loss.

One study showed that men supplementing with soy isoflavones showed increased serum equol and decreased serum DHT. If the same relationship holds true for a lotion with s-equol and scalp tissue DHT, then s-equol might help lower scalp DHT, and make for a great ingredient in a hair loss-fighting topical.

In fact, one hair loss sufferer active on some hair loss forums claims to show photographic improvements from combining mechanical stimulation (PDO needle threads) and his own homemade equol topical. See these photos (they’re often confused as before-after photos for Brotzu Lotion, but they aren’t):

(source)

Going into the science behind how S-equol reduces DHT is out-of-scope for this article. If you’d like a more in-depth analysis, feel free check out part one of this Master Guide For Reducing DHT. It covers the science behind S-equol, and every major “angle of attack” for reducing DHT for the purpose of improving hair loss.

We can think of topical S-equol like a topical finasteride (Propecia). While S-equol and finasteride work through different mechanisms, they both help reduce DHT levels.

According to Dr. Brotzu, S-equol makes Brotzu Lotion 80% more effective — likely due to its synergies with the lotion’s final (and critical) ingredient: a fatty acid known as dihomo-gamma-linoleic acid (DGLA).

Ingredient #3: Dihomo-Gamma-Linoleic Acid (DGLA)

DGLA is a type of polyunsaturated fat, and specifically, an omega six fatty acid.

Omega six fatty acids have a bad reputation in certain hair loss circles (like Ray Peat). For years, I wrote off most omega six fatty acids as “generally problematic”. But a reevaluation of the literature suggests that certain omega six fatty acids may be beneficial not only for our health, but also for our hair.

DGLA may be one of the good guys. There’s an overwhelming amount of evidence supporting its benefits.

For starters, people who are DGLA-deficient tend to develop significantly more inflammatory-based conditions — like diabetes, atopic dermatitis, rheumatoid arthritis, cancer and cardiovascular disease.

This is probably because DGLA tends to exert broad anti-inflammatory effects. It also helps slow cell growth, and some researchers even think DGLA could enhance the effectiveness of certain cancer treatments.

…But How Might DGLA Improve Hair Growth?

Interestingly, DGLA’s anti-inflammatory, anti-tumor benefits are attributed less so to the fatty acid itself… and more so to what DGLA turns into inside our bodies: something called prostaglandins…

…and interestingly, prostaglandins and hair loss are closely connected.

The Prostaglandin-DGLA-Hair Loss Connection

Prostaglandins are substances our bodies make from polyunsaturated fats (omega 3’s and 6’s). They help our tissues recover from injuries and infections. And there are so many prostaglandins (prostaglandin D2 (PGD2), prostaglandin E1 (PGE1), prostaglandin F3 (PGF3), etc.) that scientists need a lettering-numbering system built around their molecular structures to keep track of them all.

In general, different prostaglandins exert different effects. Some prostaglandins are pro-inflammatory; others are anti-inflammatory; others are both.

And interestingly, certain prostaglandins linked to chronic inflammation are also linked to pattern hair loss. Here’s how.

The “Bad” Prostaglandin: Prostaglandin D2 (PGD2)

Prostaglandin D2 (PGD2) is a pro-inflammatory prostaglandin, and studies show that PGD2 is chronically elevated in balding scalps. For unknown reasons, PGD2 seems to stop hair follicle stem cells from becoming progenitor cells — a critical step in hair follicle development (and the hair cycle). The end-result: a decrease in hair lengthening in mice and humans — or in other words — hair shortening.

This is typically one of the first signs of pattern hair loss: slower-growing hair. And once that hair disappears and fibrosis (scar tissue) sets in, it becomes a lot harder to regrow. This is why PGD2-reducing drugs like Setitpiprant are currently undergoing hair loss trials for FDA-approval. The hope: if we can reduce the presence of this “bad” prostaglandin, maybe we can regrow some of the hair that was lost.

But interestingly, not all prostaglandins are bad. In fact, some prostaglandins are considered “pro-hair” — mainly because of their anti-inflammatory properties. And just how researchers are developing drugs to decrease the “bad” PGD2, they’re also developing drugs to increase the “good” prostaglandins.

Enter prostaglandin E1 (PGE1): a prostaglandin that reduces inflammation, expresses near healthy hair follicle sites, and is also the current target (and attention) of a few pharmaceutical companies trying to create a new hair loss treatment… including Brotzu.

The “Good” Prostaglandin: Prostaglandin E1 (PGE1)

That fatty acid in Brotzu’s formula — DGLA — is a precursor to PGE1. In other words, DGLA is what our bodies use to make PGE1. The more DGLA, the more PGE1, the better our chances for healthier hair.

DGLA Increases PGE1, Which May Improve Our Hair

According to Dr. Brotzu’s patent, prostaglandin (PGE1) may help our hair in three ways:

1. PGE1 decreases DHT — it inhibits the enzymes that convert free testosterone into DHT
2. PGE1 is a vasodilator — it increases blood flow
3. PGE1 increases angiogenesis — it encourages the formation of new blood vessels

In fact, Dr. Brotzu argues that PGE1 may improve microcirculation better than minoxidil (Rogaine). In this interview, he states that PGE1 stimulates not just one — but both — types of cells that interact to form our blood vessels: endothelial cells (the inner lining of our vessel walls), and pericytes (the smooth muscle “surface” of our blood cells). According to Dr. Brotzu, minoxidil (Rogaine) only affect pericyte cells — making it less effective.

Should We Try To Make Our Own Brotzu Lotion? No.

Brotzu Lotion isn’t yet slated for a US release, and as a result, some hair loss sufferers are trying to organize group buys to make the topical at home.

But while Dr. Brotzu’s patent theoretically gives you everything needed to make the Brotzu Lotion, there’s still a lot that can go wrong with the DIY approach.

Here are the two biggest problems.

Problem #1: DGLA Isn’t Widely Available

DGLA is only found in trace amounts in mammals. It also isn’t commercially available in the US (to my knowledge). That means that you can’t buy it. You can, however, buy gamma-linoleic acid (GLA). And GLA is the precursor to DGLA.

GLA is abundant in plants, human breastmilk, and herbs like borage (and thereby borage oil). And humans seem to convert GLA into DGLA in a dose-dependent manner — meaning that if we eat more GLA, we’ll make more DGLA, and theoretically, we’ll make more PGE1.

You might be thinking, “If GLA turns into DGLA, and DGLA turns into PGE1 — then what difference does it make? Why can’t I just buy GLA to increase my PGE1 levels?”

Well, inside our bodies, DGLA can turn into one of two things: arachidonic acid, or prostaglandin E1. See this chart below — which represents the different metabolic pathways polyunsaturated fats take in our bodies.

As you can see, what happens to a polyunsaturated fat depends on its molecular structure (omega 3, omega 6, etc.) — and the source of the polyunsaturated fat (i.e., if it’s plant-derived, shellfish-derived).

What’s relevant below: the orange boxes (and their flowcharts).

(source)

Keep in mind: Dr. Brotzu’s lotion is formulated to encourage the conversion of DGLA into PGE1. But if we blindly supplement with GLA — hoping it will all convert into DGLA — this may not always happen.

In fact, some percentage of GLA will become something called arachidonic acid — which is the precursor to the “bad” prostaglandin PGD2.

In other words, taking DGLA blindly or without the right adjuncts may increase both PGE1 and PGD2, which may have a neutral or negative overall effect on our hair.

Interestingly, among human populations, the following factors of GLA consumption vary wildly:

1. Our ability to convert GLA into DGLA
2. The percent of DGLA we convert into PGE1
3. The percent of DGLA we convert into arachidonic acid

…and to make matters more confusing, those percentages also change depending on which part of the body we’re studying!

Researchers believe that the above is mostly determined by our genes — and specifically, our expression of genes that help produce the enzymes required to convert GLA into DGLA, and DGLA into all of its byproducts.

Interestingly, this may also be the reason why a small percentage of Brotzu Lotion testers are seeing amazing results — and in just a couple of months. They may have the genes needed to better metabolize the topical — which might explain why their hair regrowth is dramatically better than most other users.

Problem #2: Stability

The ratios of Brotzu Lotion’s ingredients matter, and anecdotes from both Dr. Brotzu and hair loss forum “group buys” suggest that it’s very hard to keep the formula stable.

In fact, some speculate this could be why it’s taking longer than expected for Pharma Fidia to release Brotzu Lotion in Europe. It seems like every few months — the latest expected release date passes.

Brotzu Lotion For Hair Loss: Key Takeaways

Brotzu Lotion contains S-equol, DGLA, and propionyl-l-carnitine. Together and in the right ratios…

• S-equol helps reduce free testosterone (and thereby DHT)
• DGLA turns into PGE1, which helps increase blood flow and reduce DHT
• Propionyl-l-carnitine enhances the penetration and metabolism of both S-equol and DGLA

In a way, we can think of Brotzu Lotion like a safer topical finasteride + minoxidil. After all, finasteride (Propecia) reduces DHT. Minoxidil (Rogaine) increases blood flow and may increase PGE. And Brotzu Lotion? It decreases DHT, improves blood flow, and increases PGE1 — but through entirely different mechanisms than finasteride and minoxidil… and without any reported side effects (so far).

Brotzu Lotion shows significant promise for autoimmune hair loss conditions like alopecia areata — probably because it targets inflammatory biomarkers involved in the early stages of alopecia areata onset.

Brotzu Lotion also shows some potential for pattern hair loss (androgenic alopecia), but nothing worth getting too excited about. A six-month study shows the lotion helps stop pattern hair loss, with only marginal visual improvements to hair growth. Any claims of “reversing the balding clock by five years” have yet to be proven.

Having said that — there seem to be a few pattern hair loss sufferers who respond very well to the formula. These users likely have the right genes / gene expression to metabolize high amounts of DGLA into PGE1, and as a result, get more out of the topical’s mechanisms of action. In addition, these users may also have suffered from rapid-onset AGA (aggressive pattern hair loss in a few months or years). In rapid-onset AGA, balding areas are more so affected by PGD2-induced hair shortening, and less so affected by scar tissue development (since that happens later). As such, a rebalancing of prostaglandin expression in balding tissues (which is what Brotzu Lotion helps to do) may be all these users need to see hair recoveries — since scarring has yet to settle in for them.

Scarring is also likely why Brotzu Lotion works better for alopecia areata than androgenic alopecia. Alopecia areata isn’t typically a scarring form of hair loss, whereas androgenic alopecia may be a scarring form of hair loss – and potentially mediated by a combination of genetics, chronic tension, androgens, and chronic inflammation.

Questions? Comments? Thinking of trying Brotzu Lotion when it’s available? Feel free to leave a comment below. I do my best to get back to everyone.

Is Small Intestinal Bacterial Overgrowth (SIBO) Connected To Hair Loss?

Not long ago, I wrote an article about the connection between acne and hair loss (androgenic alopecia), and highlighted research suggesting that a primary driver of acne (specifically, acne rosacea) may be a condition known as small intestinal bacterial overgrowth (SIBO).

This got a lot of readers asking: is SIBO also related to hair loss? And if so — how do I test for small intestinal bacterial overgrowth… and how do I resolve it?

The answers aren’t straightforward. For one, I haven’t found a single paper demonstrating a clear connection between hair loss and SIBO. However, several papers suggest a connection between SIBO and intestinal inflammation, nutrient malabsorption, and the over-colonization of gram-negative bacteria… all of which are involved in the pathology of fibrosis (ie: scar tissue development) and certain fibrotic disease states (ie: cystic fibrosis). And as we know, fibrosis is directly implicated in the pathology of pattern hair thinning.

But we’re stretching the evidence here. We can’t conclude that just because SIBO is linked to cystic fibrosis — then it must also be linked to all forms of fibrosis — like the kind implicated in pattern hair loss (perifollicular fibrosis)…

But anecdotally, the SIBO-hair loss connection gets more interesting.

Of the female hair loss sufferers with whom I’ve worked — nearly every woman who tested for SIBO, tested positive. And of the women who sought SIBO treatment and later retested as SIBO-negative, those women reported a reduction in hair shedding, and that their hair (which in some cases, had stopped growing) started to lengthen again.

Those are huge wins — especially for any female hair loss sufferer who feels she’s exhausted her hair loss treatment routes and doesn’t know where to turn next. And while SIBO doesn’t seem as prevalent in male hair loss sufferers — at least the ones with whom I’ve worked — the reality is this: anything that contributes to chronic inflammation in the small intestine (ie: SIBO) has the potential to hurt our hair.

Why? Because the small intestine is roughly 20 feet long. And of the foods we eat, it’s responsible for nearly all nutrient absorption. That includes iron, vitamin B-12, and vitamin D — of which many female hair loss sufferers are deficient. Dozens of studies show that prolonged protein malabsorption and nutrient deficiencies can lead to diffuse hair thinning, excessive hair shedding (telogen effluvium), and even autoimmune-related hair loss like alopecia areata.

And encouragingly, studies also show that resolving these deficiencies — either with better nutrition, or fixing the underlying causes of malabsorption (like SIBO) — might sometimes lead to hair recovery (see these articles on vitamin D and zinc).

So… If I Have SIBO And Treat It, Will I Regrow My Hair?

Now, this doesn’t suggest that for the majority of those with hair loss — treating SIBO will regrow hair. But it does suggest — for men and women who fit the bill of SIBO symptoms — that resolving SIBO might also help resolve some of the underlying factors associated with their hair loss… and in doing so, maybe slow or stop hair loss (or encourage healthier hair growth).

So how do we test for small intestinal bacterial overgrowth? And if we test positive, how do we resolve it?

SIBO Treatment Recommendations Vary Wildly

There are many kinds of SIBO, and each kind requires a different treatment. Depending on the doctor — everyone seems to have differing opinions on how to best treat each SIBO type.

Resolving SIBO is also complicated, and it’s something of which I lack first-hand experience (I tested SIBO-negative in a breath test two months ago). Moreover, there’s limited research on SIBO pathology and treatment efficacy. As a result, SIBO sufferers often must rely on the experience and advice of medical professionals who work with SIBO patients regularly.

The bottom line: I’m a hair loss researcher, not an SIBO expert. And that means you shouldn’t read about SIBO treatments from me; you should read about them from someone more qualified. So I decided to forgo writing the rest of this article — and instead reach out to an authority in digestive health.

I’d like to introduce John Brisson — an author, researcher, educator, and expert in digestive disorders, hormone dysregulation, autoimmunity, and most importantly: small intestinal bacterial overgrowth.

John is the cofounder of fixyourgut.com. His deep-dive into health research began from a personal tragedy. His experience working with SIBO and digestive disorder sufferers spans years and thousands of hours. And today, he’s even referred to as a contributor and expert in published medical literature.

Note: I am not financially affiliated with John Brisson or his website. But I’ve spoken with him over Skype, and I value his work. There are few others qualified to write the same SIBO treatment guidelines, and my hope is that this content will help anyone who might be experiencing SIBO, hair loss, or both.

So let’s get started. John’s content covers what is SIBO, why SIBO negatively impacts our health, how to test for SIBO (and minimize false results), and most importantly: how to treat SIBO based on its type (methane-dominant, hydrogen-dominant, or both).

—

Note: the following is written by John Brisson of fixyourgut.com

SIBO, Gut Health, And Bacterial Overgrowths

Bacterial dysbiosis (a microbial imbalance of bacteria inside the body) can wreak havoc on many different aspects of our overall health. I have coached many people with SIBO, and I have seen those with the condition struggle trying to manage their illness and the stress of modern life. Imagine reacting negatively to almost everything you consume, causing severe abdominal distension to the point where you look like you are pregnant, for weeks and months at a time.

SIBO (small intestinal bacterial overgrowth) is a medical condition where many people have an opportunistic bacterial infection in the small intestine. And unfortunately, SIBO can take a serious toll on one’s physical, social, spiritual, and mental health because it directly compromises the functionality of the small intestine.

Why Is The Small Intestine So Important?

The small intestine helps to break down proteins, lipids, and simple carbohydrates and is very important for the assimilation of nutrients. The MMC (migrating motor complex) maintains peristalsis in the small intestine and helps move our food along for proper digestion.

With a bacterial overgrowth in the small intestine, our ability to process and absorb nutrients is significantly impaired, and will remain so until the condition is addressed.

What Causes SIBO?

The development of SIBO is usually caused by the poor standard American diet, food poisoning, viral gastroenteritis, antibiotic overuse, motility issues (mainly chronic constipation), or long-term use of stomach acid reducing medications (proton pump inhibitors or antacids).

The long-term use of acid-reducing medications causes opportunistic bacteria that would typically be eliminated by stomach acid, to survive and flourish in the small intestine. A lack of stomach acid causes food proteins to become partially undigested. Allergies develop from the undigested proteins.

Undigested proteins also cause excessive flatulence and increase inflammation. The standard American diet of FODMAP carbohydrates allows opportunistic bacteria to thrive, strongly colonize the small intestine, and produce excess gas.

How Does SIBO Develop?

These contributing factors create a window of opportunity for microorganisms to enter and colonize the small intestine, an organ with relatively fewer microorganisms than the rest of our intestinal tract. This leads to something known as opportunistic dysbiosis (a microbial imbalance), which depending on the severity, begins to inhibit the small intestine’s ability to perform its tasks.

The more opportunistic bacteria in our small gut, the more food that bacteria ferments, and the more gas byproducts and toxins they produce.

The opportunistic microorganisms (and their toxic byproducts) then begin to decrease fat absorption in the intestines. This leads to stool problems with color/fat content. And unfortunately, the cycle reinforces itself. Increased fermentation in the small intestine also increases the chances of further small intestinal dysbiosis, and as a result, the intestinal lining further degrades and eventually cannot digest larger nutrients correctly.

These improperly digested start to cause food allergies and sensitivities.

The opportunistic microorganisms produce toxins that then enter the bloodstream from the loss of integrity in the intestinal wall. Excessive toxins in the bloodstream lead to an immune overreaction that causes fatigue, systemic joint pain, and elevated liver enzymes.

Finally, these byproducts or toxins that cause neurological and cognitive problems including cognitive impairment and forgetfulness. The vicious cycle continues as the body’s immune system tries to eliminate the opportunistic microorganisms, which react to the body’s defenses by releasing more acids, toxins, and creating more opportunities for these inflammatory microorganisms to continue to flourish. The cycle then repeats itself, and the end result is chronic illness.

What Are The Symptoms Of SIBO?

The main symptoms of a SIBO infection are indigestion, an increase in flatulence, and horrible-smelling deification, burps, and flatulence. Other symptoms of SIBO include abdominal pain, severe bloating, abdominal distention, chronic constipation, acid reflux (GERD), fatigue, headaches, chronic diarrhea, fat malabsorption, food allergies, and occasional low-grade fever. There is also a strong correlation between rosacea and SIBO.

In my coaching experience. I’ve found that most people with IBS (irritable bowel syndrome) are actually suffering from SIBO, and that SIBO is their main cause of their digestive problems.

Diagnosing SIBO: The Hydrogen/Methane Breath Tests

A hydrogen/methane breath test is often the standard used to diagnose SIBO.

The hydrogen/methane breath test is a non-invasive fasting test in which your doctor has you breathe into a machine that monitors excess hydrogen or methane that is released by the opportunistic bacteria in your small intestine.

You are given glucose, dextrose, or lactulose, during the test to consume, and the test input is collected at twenty-minute intervals for at least three-five hours.

SIBO-Positive Thressholds

If you produce at least twenty ppm of hydrogen or three ppm of methane during the test, you test positive for an active SIBO infection (but even a result of twelve ppm hydrogen should be treated at the very minimum).

If your hydrogen and methane are flat-lined or do not rise during the test, you may have the third type of SIBO: hydrogen sulfide producing bacterial overgrowth.

SIBO Tests Aren’t Perfect! Sugars & False Results

It’s debatable which sugar is best to ingest for diagnosing SIBO (lactulose or glucose). For instance, bacteria have to ferment lactulose in the intestines for it to be absorbed by the body. Glucose is easily broken down by the microbiome or directly absorbed by the gastrointestinal system.

Moreover, the use of glucose as a test marker may give a false negative reading because at least seventeen feet of the small intestine may not be tested. And in people with irritable bowel syndrome with diarrhea (IBS-D), the glucose might reach the cecum and begin fermentation sooner, creating a false positive SIBO result in people with strictly colonic overgrowth.

There are also issues with the use of lactulose that might produce false negatives. Not all organisms that cause an overgrowth ferment lactulose, and if you have an overgrowth of bacteria that doesn’t ferment lactulose, you might receive a false negative test result. In addition, lactulose increases bowel transit time, which can further skew test results. So if you’re going to test for SIBO, you need to be aware of these issues so that you can maximize your chances for an accurate diagnosis.

Want To Get Tested For SIBO?

I recommend using these guidelines of hydrogen/methane breath interpretation by the leading SIBO expert, Dr. Allison Siebecker. I also recommend getting a GI Effects performed by Genova Diagnostics through your gastroenterologist.

You can find out how to order the SIBO tests (based on your location) right here.

It might be best to get both tests done (glucose and lactulose) to determine bacterial overgrowth, alongside that bowel transit test as well, to determine one’s motility and how long it would take the test substances to reach the colon. That way, you’ll have a better idea of what’s going on (and help minimize your chances of an incorrect diagnosis).

And remember, some people can have SIBO symptoms and still receive a negative diagnosis. This is because not every overgrowth of bacteria in the gut will contain bacteria that produce hydrogen.

There is also no unified medical interpretation of SIBO breath tests. Therefore, a doctor might perceive your results to be normal, and they aren’t. If your values do not rise during the test, you may have hydrogen sulfide producing bacterial overgrowth in the small intestine.

How Do You Treat SIBO? It All Depends…

So, what do you do if you have SIBO? In general, it’s better try an SIBO treatment if you have many of its symptoms, instead of relying on an unpredictable diagnosis from breath testing.

Depending on the type of SIBO you have, some doctors might prescribe antibiotics including Xifixan, Cipro, Flagyl, or Neomycin. Some more integrative doctors may prescribe more natural approaches like Allison Seibacker’s natural protocol for tackling SIBO.

Many people follow a low FODMAP diet to try to reduce overgrowth and control symptoms with moderate success (if you’re interested, here are specific guidelines).

If you are not any better within a month of following a low FODMAP diet or doing any SIBO protocols, then SIBO was either not your problem in the first place (it could be small intestinal yeast overgrowth (SIYO)), or the protocol was not strong enough to eliminate some of the hardier bacteria like MAP (Mycobacterium avium paratuberculosis, a cause of Ulcerative Colitis and Crohn’s disease) or Klebsiella (a cause of Rheumatoid Arthritis and Ankylosing Spondylitis).

If you find yourself in the latter position, you should know there’s currently no public test for MAP (outside of specific testing at a university or hospital pathology laboratory), but Klebsiella can be tested for by using Genova’s GI Effects Stool Profile test (you’ll need a gastroenterologist to order the test, though some functional medicine practitioners can order these too).

SIBO Treatment Guidelines

Treating Hydrogen-Producing SIBO

If you are suffering from hydrogen producing SIBO, taking the antibiotic Xifixan for ten to fourteen days, or following my hydrogen SIBO protocol for two to four weeks, may help reduce your overgrowth and improve your digestion.

In addition, many of my clients with dominant hydrogen overgrowth have seen success with using berberine and oil of oregano as antimicrobial agents, and activated charcoal to help with loose stools. Moreover, following a low FODMAP diet for a few weeks may help reduce bloating.

Treating Methane-Producing SIBO

If you are suffering from methane-producing SIBO, following my methane dominant SIBO protocol for two to four weeks may help reduce your overgrowth and improve your digestion.

Many of my clients with dominant methane overgrowth have seen success with using allicin, neem, or Atrantil as antimicrobial agents and magnesium and 5-HTP to help increase motility. Multiple protocols and rotation of herbs may be needed for proper recovery, as most your gut issues didn’t start overnight, and it might take some time for your digestion to improve.

Above all, don’t become discouraged. Most people improve their quality of life or conquer their SIBO in time.

—

Note: the above segment is written by John Brisson of fixyourgut.com

Read time: 10 minutes

Note: this is part three of a four-part series — a master guide to reducing DHT levels for hair loss. Missed the earlier articles? Read part one here, and part two here.

Summary So Far: Decrease DHT With Free Testosterone, 5-Alpha Reductase

In the first article, we uncovered what DHT is, how it’s made, the DHT-hair loss connection, and how we can reduce DHT (and maybe fight hair loss) by using four major levers.

1. Decrease free testosterone
2. Inhibit 5-alpha reductase
3. Decrease androgen receptors
4. …and one more we’ll reveal in the next article

Then we dove into all the mechanisms by which we can decrease DHT by using the first and second lever: reducing free testosterone and inhibiting 5-alpha reductase.

By the end of the second article, we summarized the mechanisms (but not all the drugs, foods, supplements, and treatments) targeting those first two levers:

But we still have two DHT-fighting levers left.

1. Decreasing androgen receptors, and…
2. A mystery lever (for the next and final article…)

This article is the third installment to our DHT-reducing mechanism series. We’ll uncover the third major DHT-reducing pathway – and its known mechanisms – in hopes of reducing DHT to slow, stop, or reverse pattern hair loss.

It all builds into our Master Flowchart: A Guide To All Major DHT Reducing Mechanisms To Fight Against Hair Loss.

What we’re covering now: decreasing DHT by reducing androgen receptors. And the research here is pretty exciting (at least to me).

Reduce DHT By Decreasing Androgen Receptors

What Are Androgen Receptors?

Androgen receptors are the places inside a cell where androgens (testosterone, DHT, etc.) attach themselves. After an androgen attaches to an androgen receptor, these androgens can then influence a cell’s function.

Remember: DHT forms when free testosterone interacts with the enzyme type II 5-alpha reductase and converts that free testosterone into DHT. Then that DHT binds to a cell’s androgen receptor, where it influences that cell (and tissue). In the case of pattern hair loss, the kind of DHT people want to reduce is scalp tissue DHT.

Think of androgen receptors like a landing pad for DHT. Without an androgen receptor, DHT can’t attach to the cell and influence its function. And in the case of pattern hair loss – without androgen receptors, DHT can’t attach to scalp tissue DHT (the kind of DHT associates with hair thinning).

How Can We Decrease Androgen Receptors?

There are at least three ways to decrease influence receptors…

1. Decrease total androgen production
2. Decrease androgen receptor expression
3. Block androgen receptors

Let’s dive into all three. We’ll give a few examples pertaining to each pillar, but this article is by no means an exhaustive list of strategies.

#1: Decreasing Total Androgen Production

We’ve actually covered this method before – albeit for reducing DHT via free testosterone. And to reiterate: this is a bad idea.

For instance, one way of blocking our body’s ability to produce androgens (and thereby reducing androgen receptor expression) is castration. Another way is to take drugs that change the brain signaling pathways in our hypothalamus so that our bodies convince themselves they need to produce less testosterone to thrive.

Yes, blocking total androgen production significantly decreases androgen receptor activity (likely because there are fewer total androgens available). But doing so comes attaches to serious side effects. And the costs of these side effects far outweigh any benefit to DHT reduction and hair health.

The consequences of this kind of DHT-reducing approach? Low/no libido, depression, sexual dysfunction, the list goes on. So when it comes to safely decreasing androgen receptors, please consider all other options aside from reducing total testosterone production.

In any case, here’s what this looks like in a flowchart:

Fortunately, there are other ways to target DHT by reducing androgen receptors. For instance: decreasing androgen receptor expression.

And this is where it gets interesting.

#2: Decreasing Androgen Receptor Expression

When we talk about decreasing androgen receptor expression, we’re not talking about manipulating androgen receptor activity by taking away the thing that tells our bodies to activate them – the androgens themselves. Instead, we’re talking about changing the actual environment of our tissues – so that fewer androgen receptors activate in those tissues.

One potential way to decrease androgen receptor expression?

Increase tissue oxygen levels.

Hypoxia (Oxygen Restriction) Increases Androgen Receptor Activity

In the prostate, reduced oxygen levels – in combination with DHT – dramatically increases androgen receptor activity. In fact, it increases androgen receptor expression six-fold versus DHT alone.

Why is this interesting? Well, an enlarged prostate and men’s balding scalps have a lot in common.

For one, our prostates and our balding scalp regions both use the enzyme type II 5-alpha reductase to convert free testosterone into DHT – and not other forms of 5-alpha reductase.

In addition, high DHT levels are associated with both balding scalp regions and an enlarged prostate.

But even more interesting? Hypoxia (lower oxygen) is associated with both prostate cancer and regions of the scalp which are balding.

Could the increased DHT we see in balding scalps somehow be connected to hypoxia? Possibly. Especially when we consider how androgen receptors, in the presence of DHT and hypoxia, express 6-fold higher than in the presence of DHT alone.

What does all this mean? We can probably reduce DHT levels by decreasing androgen receptor expression. And how can we do that? By increasing oxygen tissue levels.

If We Increase Scalp Tissue Oxygen, Can We Reverse Hair Loss?

The evidence on oxygen therapies, DHT levels, and hair growth in humans is essentially non-existent. So, we don’t know.

Anecdotally, I’ve spoken with two people who tried hyperbaric oxygen therapy and said that it regrew their bald vertexes over a period of four months. And there’s also a patent on injectable ozone for hair loss sufferers, with cited case studies.

With that said, there’s not enough evidence to say that increasing oxygen is a viable option for 1) reducing androgen receptors, 2) reducing DHT levels, or 3) regrowing hair. There are anecdotes, but no hard data.

Another challenge with oxygen: delivery. Just because we inhale pure oxygen doesn’t mean we actually raise tissue oxygen levels. This is probably why future hair loss therapies using oxygen will come in the form of injections rather than hyperbaric chambers – if at all.

But the bottom line: if we increase tissue oxygen levels, my bet is that this will 1) decrease androgen receptor activity and 2) encourage hair regrowth.

So let’s summarize our mechanisms (so far) for decreasing androgen receptors:

This brings us to our last mechanism to reducing androgen receptors: blocking them. And if you’ve tried many hair loss drugs or keep up with hair loss research, there’s a good chance you know what’s coming.

#3: Blocking Androgen Receptors

What does it mean to block androgen receptors?

In simple terms, it means to bind something to an androgen receptor so that the androgen receptor is “blocked off” from binding with actual androgens, like testosterone or DHT.

That’s how androgen receptor blockers reduce DHT: the AR blockers bind to a cell’s androgen receptors and prevent DHT from binding to that same cell. In effect, that DHT can no longer influence that cell’s function.

Androgen receptor blockers come in two forms: steroidal and non-steroidal. And like steroidal 5-alpha reductase inhibitors, steroidal androgen receptor blockers are also synthesized from hormones like progesterone.

#1: Steroidal Androgen Receptor Blockers – Spironolactone

When it comes to hair loss (and reducing DHT), a popular androgen receptor blocker among women is a drug called spironolactone (branded as Aldactone). This is an androgen receptor blocker derived from the hormone progesterone.

Spironolactone reduces DHT by blocking androgen receptors, and doctors often prescribe this drug in oral form for women suffering from female pattern hair loss or even hirsutism – unwanted body and facial hair growth. This is because increased DHT is associated with hair loss in the scalp, but ironically, hair growth in the body and face.

Spironolactone is a powerful anti-androgen. In fact, most men are advised against taking it orally as a hair loss treatment. Why? It can be feminizing. In fact, oral spironolactone is the same drug some men use to transition genders and become female.

However, spironolactone also comes in topical form – so we can concentrate its anti-androgen receptor effects to our scalps and minimize the risk of feminization.

#2: Non-Steroidal Androgen Receptor Blockers – RU58841

Aside from not being derived from hormones, the major difference between steroidal vs. non-steroidal androgen receptor blockers is that non-steroidal AR blockers are what we call “silent” androgen receptor antagonists. In other words, they block androgen receptors without actually activating them.

Two examples of non-steroidal androgen receptor blockers for hair loss?

1. Flutamide. Historically, this drug was mostly geared for female pattern hair loss sufferers and men with advanced stage prostate cancer. But recent advents in topical delivery via nanoparticles might make this drug effective for hair loss – and maybe even devoid of major side effects.
2. RU58841. In the past few years, RU58841 made the rounds on hair loss forums, but it has yet to legally make it to the US market (technically, you can still get your hands on it – albeit for “research” purposes only).

The side effects of non-steroidal androgen receptor blockers aren’t fully understood, so unfortunately I can’t say much. What I will say: when it comes to any anti-androgen – do your research, understand the risks, and exercise caution.

Now let’s add all of this to a flowchart:

Reduce Androgen Receptors: Summary

When it comes to reducing DHT by decreasing androgen receptors, there are three major ways we can go about doing this:

1. Decrease total androgen production
2. Decrease androgen receptor expression
3. Block androgen receptors

Here’s a summary of the major mechanisms behind each way:

Again, this article series is only here to present a handful of angles and mechanisms for DHT reduction; it’s not here to compare these angles against one another (as most of them haven’t been studied for the treatment of pattern hair loss).

In any case, let’s add these discoveries to our master flowchart, which is just one article away from completion. (The chart is getting big, so click on it to enlarge.)

What’s Next…

When it comes to reducing DHT in hopes of stopping hair loss, we’ve covered…

• Free Testosterone
• 5-Alpha Reductase
• Androgen Receptors

But there’s still a fourth DHT-reducing pillar we haven’t discussed. What is it?

Increasing DHT metabolism.

In fact, research in increasing DHT metabolism might hold promise for hair loss sufferers looking to decrease scalp tissue DHT but avoid the sexual side effects of DHT reduction. This is all covered in the next (and final) article – where we will complete our Master Guide To The Mechanisms Behind DHT Reduction.

Read time: 10 minutes

Note: this is part two of a four-part series — a master guide to reducing DHT levels for the purpose of fighting hair loss. Missed part one? Read it right here.

Part One Summary – Decreasing DHT By Reducing Free Testosterone

In the last article, we uncovered what DHT is, how it’s made, the DHT-hair loss connection, and the four major levers to reduce DHT levels in hopes of stopping hair loss:

1. Decrease free testosterone
2. Inhibit 5-alpha reductase
3. Decrease androgen receptors
4. …and one more we haven’t yet revealed

Then we dove into all the ways we can decrease DHT by using that first lever: reducing free testosterone. Here’s a summary of the mechanisms (but not all the drugs, foods, supplements, and treatments that target these mechanisms):

Unfortunately, most of these approaches are bad ideas. For instance – yes, we can theoretically plummet DHT production via castration. And yes, castration has been shown to significantly slow or stop pattern hair loss. But for most men, the consequences of castration far outweigh the pain of losing our hair.

So when it comes to reducing DHT by decreasing free testosterone, we don’t have many viable options…

The good news? There are still three other levers of attack against DHT.

The one we’ll cover inside this article: inhibiting the enzyme 5-alpha reductase.

Part Two: Decreasing DHT By Inhibiting 5-Alpha Reductase

Review: Three Levers Of DHT Reduction

Remember: in order for dihydrotestosterone (DHT) to form, we need all of the following present:

1. Free testosterone
2. 5-alpha reductase
3. Androgen receptors

As a result, this gives us three major levers to reduce DHT levels: decrease 1) free testosterone, 2) 5-alpha reductase, and / or 3) androgen receptors.

We’ve already covered the major ways to reduce free testosterone (and thereby decrease DHT). Now it’s time to move onto the enzyme 5-alpha reductase.

What Is 5-Alpha Reductase?

5-alpha reductase is the enzyme our bodies use to convert free testosterone into DHT. And without the enzyme 5-alpha reductase, DHT cannot form (at least at relatively high quantities).

There are many types of 5-alpha reductase, but when it comes to hair loss, the one that gets the most attention is type II 5-alpha reductase.

Type II 5-alpha reductase is the enzyme expressed in our scalp skin and prostate. Some men have a rare genetic mutation where their bodies can’t produce any type II 5-alpha reductase. And interestingly enough, these men don’t go bald.

The net: we need type II 5-alpha reductase to make DHT in our scalp skin. And that means if we can reduce the expression of type II 5-alpha reductase, we can also reduce our DHT levels (and possibly prevent or partially reverse pattern hair thinning).

Which brings us to our second angle of attack against DHT…

Angle Of Attack #2: Reducing 5-Alpha Reductase

There seems to be at least two pathways to inhibiting (or reducing the presence of) this enzyme.

1. Directly (competitively inhibit 5-alpha reductase)
2. Indirectly (reduce inflammation)

Let’s take these one-by-one.

#1: Direct 5-Alpha Reductase Inhibition

Competitive Inhibition

5-alpha reductase doesn’t just arrive out of nowhere. In order for this enzyme to form and mediate the whole DHT conversion process, it needs the help of a coenzyme known as nicotinamide adenine dinucleotide phosphate… or in other words, NADPH.

5-alpha reductase needs NADPH to convert free testosterone into DHT. So an effective way to stop the formation of 5-alpha reductase (and reducing DHT) is to…

1. Compete with the coenzyme NADPH, or…
2. Block NADPH

These are two mechanisms of direct 5-alpha reductase inhibition – or for the lay person – reducing 5-alpha reductase by stopping it from forming. The hair loss drugs Finasteride and Dutasteride – two 5-alpha reductase inhibitors – appear to work in this way.

Mechanism 1: Compete With NADPH

Some research shows that Finasteride competes with the coenzyme NADPH. Finasteride’s molecules take the place of NADPH in a cell, and in NADPH’s absence, 5-alpha reductase cannot form. The end-result? Less DHT. And another 5-alpha reductase inhibiting drug – Dutasteride – seems to do the same thing (using a slightly different molecule).

Mechanism 2: Block NADPH (Or Bind To NADPH And Change Its Structure)

There’s also research showing that instead of competing with NADPH, Finasteride may instead bind to NADPH and change NADPH’s structure into a different coenzyme – one that doesn’t support the formation of 5-alpha reductase. The bottom line: free testosterone can no longer convert into DHT.

Interestingly, zinc may also reduce 5-alpha reductase and through a similar manner. Evidence suggests that zinc reduces NADPH production, thereby decreasing 5-alpha reductase activity. The less enzyme activity, the less DHT.

And that’s a (very) brief overview of how to reduce DHT levels by directly inhibiting the enzyme 5-alpha reductase.

#2: Indirect 5-Alpha Reductase Inhibition

Reduce Inflammation

Studies show there’s an association with DHT and inflammation. The net: DHT might regulate the inflammatory process. And in some tissues, increased DHT might even be a response to increased inflammation.

Hypothetically, if we can reduce inflammation, we might also reduce 5-alpha reductase activity (and thereby DHT levels).

Interestingly, reducing chronic inflammation may be an indirect way of reducing 5-alpha reductase. This is because reducing inflammation doesn’t directly inhibit 5-alpha reductase, but rather, inhibits the inflammation that signals 5-alpha reductase to arrive in certain tissues (like our scalp skin and prostates).

There are hundreds of ways to reduce chronic inflammation. But most boil down to two methods: we can either 1) take away whatever’s causing the inflammation in the first place, or 2) stop the signaling proteins that tell our bodies to send inflammatory cells to injury sites.

In the case of pattern hair loss, we don’t really know what causes chronic inflammation in our scalps. It could be scalp muscular tension, protruded bone growth, skin tightening, the arrival of DHT to genetically sensitive hair follicles, an inflammatory marker induced by DHT… the list goes on. But since we don’t know the cause, we’re more or less stuck with that second inflammation-reducing option: muting signaling proteins that channel inflammatory cells to injured tissues.

Fortunately, there are hundreds of substances that can do this. Covering each is out-of-scope for this article, so we’ll instead highlight just two.

Again, the list here is not a suggestion that you should use these methods. They’re just examples of substances that might hit these pathways.

1. #1: Pumpkin Seed Oil
   1. Antioxidants: decrease oxidation, decrease transforming growth factor beta
   2. Linoleic acid: decreases COX-2 enzyme
2. #2: Rosemary Oil
   1. Polyphenols: decreases COX-2 enzyme
   2. Volatile oils: decreases COX-2 enzyme, interleukins, and tumor necrosis factor

Recap: Direct Vs. Indirect 5-Alpha Reductase Inhibition

We can decrease DHT by inhibiting 5-alpha reductase through two major pathways: direct versus indirect 5-AR inhibition. Direct 5-AR inhibition is how steroid-derived hair loss drugs like Finasteride and Dutasteride work.

Conversely, we may be able to indirectly inhibit 5-alpha reductase by reducing inflammation in tissues. Inflammation and hair loss are closely linked, but since we don’t yet know what causes the inflammation that triggers hair loss, we’re more or less limited to reducing scalp inflammation by simply inhibiting the signaling proteins that send more inflammatory cells to those tissues. Rosemary oil and pumpkin seed oil have these anti-inflammatory properties. Unfortunately, they’re less studied in terms of hair loss, and probably aren’t as effective at stopping hair loss versus Finasteride (Propecia) or Dutasteride (Avodart).

Any Other Ways To Reduce 5-Alpha Reductase – Directly Or Indirectly?

Absolutely.

There’s evidence that polyunsaturated fatty acids like linoleic acid may act directly and indirectly on 5-alpha reductase by 1) reducing inflammation, and 2) altering lipid bilayers in cell membranes to decrease 5-alpha reductase formation.

There’s also evidence that vitamin B2- also known as riboflavin – may decrease 5-alpha reductase activity, though the mechanisms aren’t completely understood.

Even the polyphenols inside green tea may inhibit 5-alpha reductase.

The pathways these substances take to reduce 5-alpha reductase are complex, and they’re still being explored. As a result, I’ve omitted these from the flowchart until studies can confirm their exact mechanisms.

Finally – we can also reduce 5-alpha reductase activity by decreasing total androgen production. The less androgens our bodies produce, the less 5-alpha reductase is activated. This was covered in the first article about reducing free testosterone, and as a result, we won’t cover it again here.

Again, there’s very limited research on the effects of these non-drug strategies on hair loss outcomes. Nonetheless, I figured I’d mention them.

Summary Of Series (So Far)

When it comes to fighting hair loss by reducing DHT, there are four main levers of attack:

1. Reducing free testosterone
2. Inhibiting 5-alpha reductase
3. Blocking androgen receptors
4. A mystery lever (we’ll get to that soon)

In the last article, we covered the major ways of reducing DHT by reducing free testosterone, and provided some examples of the drugs and supplements which achieve this (inadvertently or not).

In this article, we uncovered how we can reduce DHT by inhibiting 5-alpha reductase – and through a variety of mechanisms.

So let’s combine what we know so far into one major flowchart. So far, we’re 2/4’s of the way to a complete DHT Reduction Master Flowchart:

Remember, the drugs and supplements listed above are just examples. These are by no means the most effective drugs and supplements within their respective categories, nor are they the only drugs or supplements that can achieve these effects. This flowchart is educational and not endorsing of any specific treatment.

What’s To Come…

The third installment of a Master Guide To The Mechanisms Behind DHT Reduction uncovers how to decrease DHT by decreasing androgen receptors.

Anyone researching or experimenting with additional ways to reduce 5-alpha reductase? Leave a comment! I respond to everyone.

Read time: 10 minutes

Reducing DHT For Hair Loss

When it comes to decreasing dihydrotestosterone (DHT) to slow or stop hair loss, most people only know one way to do it: inhibit the enzyme 5-alpha reductase.

But did you know we may also be able to lower DHT using bacteria? Or blocking androgen receptors? Or increasing DHT metabolism? Or maybe even decreasing inflammation, increasing tissue oxygen, and upping the presence of large protein molecules in our blood?

That’s why I wrote this article series. You’ve probably read click-bait hair loss articles about a certain drug, food, supplement, or regimen that claims to reduce DHT levels. But have you ever wondered how these treatments reduce DHT levels? By the end of this series, you’ll no longer have to ask this question.

We’re going to dive into all of the best (and worst) ways we can fight DHT in hopes of slowing, stopping, or reversing pattern hair loss.

We’ll start with the DHT-hair loss connection, and by the end, we’ll uncover…

• The FOUR major angles of attack against DHT – free testosterone, 5-alpha reductase, androgen receptors, and DHT metabolism
• The MECHANISMS behind each angle – and where things like bacteria, inflammation, and oxygen come into play
• The drugs, foods, and supplements targeting each mechanism – and which to avoid
• The truth: should we actually target DHT to reverse hair thinning? Maybe, maybe not.

The objective: to create a Master DHT Reduction Flowchart. This is a systematic, scientific overview of nearly all the conventional (and unconventional) ways to reduce DHT. Some mechanisms might help reduce hair loss… most won’t. But by the end, you’ll have a concrete understanding of all DHT-reducing possibilities.

This way, the next time you read an article about a certain “DHT blocker” or “DHT reducer” – you’ll instantly understand how it works, if it’s effective against hair loss, and what the dangers are (or aren’t) of trying it.

This series is educational. I do not endorse any specific mechanism as the “best” method. As you’ll see – especially in this article – some of these mechanisms are downright horrifying.

In any case, let’s get started. Our focus for this article: reducing DHT by reducing free testosterone (more on this soon).

The DHT-Hair Loss Connection

Why Focus On DHT For Hair Loss?

Since the discovery of testosterone in 1935, researchers have believed that androgens (like testosterone or DHT) play some sort of role in pattern hair loss. Their rationale? Men bald more often than women, and coincidentally, men have much higher androgen levels.

It didn’t take long for these beliefs to be confirmed. First, there was an observational study on men castrated before puberty. The findings: if a man is castrated before puberty (ie: before they start producing lots of androgens), androgen production remains suppressed throughout the remainder of his life – since the testes are responsible for producing 95% of a man’s testosterone. And interestingly, men castrated before puberty never go bald later on — possibly a result of permanently suppressed androgen production.

It was an interesting observation… But the hair loss story was still incomplete. Why? Because testosterone isn’t the only male androgen. There are other hormones made from testosterone that might be more at fault for hair loss. And if researchers wanted to create a viable treatment for hair loss, they’d need to get more specific and uncover the exact hormone causing the problem.

Then came an observational study on men with a rare genetic mutation: a type II 5-alpha reductase deficiency. This is the enzyme our bodies use to turn unbound testosterone into DHT in our scalps and prostate glands. The study’s findings: men with this deficiency suffered from poor genital development and no body hair… but they also never went bald later in life.

This narrowed the scope: maybe it wasn’t testosterone that caused hair loss… but rather DHT.

Many years later, researchers confirmed their suspicions after a breakthrough study confirmed that the hormone DHT is elevated in balding scalp regions – but not in non-balding scalp regions.

The key takeaway? It’s likely that DHT plays some sort of causal role in pattern hair loss. And if we want to reduce hair loss (or even reverse it), maybe we should try to reduce our DHT levels.

This was the basis for FDA-approved hair loss drugs like Propecia (finasteride) and off-label drugs Avodart (dutasteride). These drugs reduce DHT, and they’re clinically proven to help slow, stop, or even partially reverse pattern hair loss and hair thinning.

How Is DHT Made?

There are many conversion pathways to making DHT. But when we boil it down, all (or nearly all) DHT is made from the hormone testosterone. And for the majority of DHT creation, our bodies need these three things:

1. Free testosterone. Testosterone comes in two varieties – bound and unbound. And in order for testosterone to convert into other hormones, it needs to be unbound (free) so that it can connect with other proteins or enzymes that change its structure.
2. 5-Alpha Reductase. This is the enzyme our bodies use to convert free testosterone into DHT. When free testosterone comes into contact with the enzyme 5-alpha reductase, that enzyme converts the testosterone into DHT. Without the 5-alpha reductase, DHT can’t form.
3. Androgen Receptors. In our cells, androgen receptors are the landing pads for androgens (like DHT). After free testosterone interacts with 5-alpha reductase and becomes DHT, that DHT needs to attach to a cell’s androgen receptor in order to exert any effect on the tissue. Without androgen receptors, DHT has no home and can’t exert its effects on cells.

If we had to break this down into a crude formula:

DHT = Free Testosterone + 5-Alpha Reductase + Androgen Receptors

Reducing DHT To Fight Hair Loss: Three Angles Of Attack

You probably picked up on this, but we just laid down three angles of attack against DHT:

1. Decreasing free testosterone
2. Decreasing 5-alpha reductase
3. Decreasing androgen receptors

Why? Because without free testosterone or 5-alpha reductase – DHT can’t form. And without androgen receptors – DHT can’t exert any effect on a tissue (like, for example, hair loss).

So let’s dive into each angle of attack. This article only covers free testosterone. The next two will cover 5-alpha reductase, androgen receptors, and a lesser-known DHT reducing mechanism that very people ever consider.

DHT Attack Angle #1: Reduce Free Testosterone

Of all the ways to reduce free testosterone, there appear to be two major ones relevant to pattern hair loss. The first: increasing testosterone-binding proteins.

1. Reduce DHT By Increasing Testosterone-Binding Proteins

Remember how testosterone must be unbound (free) in order to convert into DHT? Well, if testosterone is bound, it can’t make that conversion. That means if we bind more free testosterone to certain proteins and enzymes, we can reduce the chances of free testosterone binding to the enzyme 5-alpha reductase and then becoming DHT.

Enter sex hormone binding globulin – a protein which binds to free testosterone and carries that bound testosterone throughout our blood. The benefit of this binding: this free testosterone is no longer free. And while that testosterone is bound, it cannot convert into DHT.

The Sex Hormone Binding Globulin-Hair Loss Connection

The more sex hormone binding globulin (SHBG) – the more SHBG binds to free testosterone, and the less free testosterone is available to convert into DHT.

It’s unsurprising that low levels of SHBG are seen in young women with diffuse hair thinning, or that lower levels of sex hormone binding globulin are observed in completely bald men.

The takeaway: maybe by increasing SHBG, we can decrease free testosterone, maybe decrease DHT levels, and maybe even improve our pattern hair loss.

How to Increase Sex Hormone Binding Globulin (SHBG)

There are countless foods, supplements, and drugs that help increase SHBG (and decrease free testosterone). We’re not going to cover all of them. But we are going to cover one of particular interest – a supplement known as S-Equol.

S-Equol is bacterially derived from daidzein, an isoflavone abundant in soy foods.

Isoflavones may increase the production of SHBG (sex hormone-binding globulin) in the liver and bind to biologically active testosterone. This results in the lowering of free testosterone.

The less testosterone in scalp tissue, the less likely it will be converted into DHT – theoretically reducing the risk of pattern hair loss. In fact, this has been validated.

One study demonstrated that short-term administration of soy isoflavones stimulated the production of serum equol and decreased the serum DHT (DHT in the blood).

But do soy isoflavones also decrease DHT in scalp tissues? Unfortunately, we don’t know. There haven’t yet been any studies to confirm this. And just because S-Equol reduces serum DHT doesn’t mean we can say it also reduces scalp tissue DHT. And when it comes to fighting pattern hair loss, scalp tissue DHT is what really matters.

Can Other Proteins Bind To Testosterone And Decrease DHT?

Maybe.

There are many large proteins in our blood that bind to hormones. Albumin – for example – is the largest protein in our blood, and is similar to SHBG in that it is made by the liver. However, testosterone bound to albumin can later become unbound. As such, testosterone bound to albumin is sometimes considered part of someone’s biologically “available” testosterone.

Should We Take S-Equol To Reduce DHT And Fight Hair Loss?

Until S-Equol is studied extensively for its effects on 1) scalp tissue DHT, and 2) pattern hair loss – we won’t know if it’s a viable treatment for hair loss sufferers.

Here’s a summary so far:

This is the first major way of reducing free testosterone (and thereby DHT). There’s one more, and this one comes with much higher risk: suppressing total androgen production.

Please be warned: the following is educational. I don’t endorse any of what’s about to come.

2. Reduce Free Testosterone By Decreasing Total Androgen Production

Our brain – or specifically our hypothalamus – determines how much testosterone our bodies should produce. In fact, our hypothalamus sends this message to our testes – which produce 95% of testosterone for men. Together with this messaging, the testes then synthesize testosterone from cholesterol and send it out through our bloodstream. It’s here that our testosterone then binds to proteins and enzymes – converting into different androgens and performing hundreds of bodily functions.

You might’ve already guessed it, but if we want to reduce DHT by reducing our body’s production of androgens, we just laid out three more levers:

1. Reduce androgen signaling needs from the hypothalamus
2. Reduce cholesterol (and other testosterone production-signaling biomarkers)
3. Reduce our testes’ ability to produce androgens

Let’s take these one-by-one. And please, don’t try any of these. Seriously. It’s just a bad idea.

1. Decrease Androgen Signaling From The Hypothalamus

Certain steroids and drugs can reduce our body’s desire (or ability) to produce testosterone. For example, steroids known as corticosteroids – through unknown mechanisms – can reduce the amount of testosterone our bodies decide to produce. This may be due to the drugs muting androgen signaling needs from our hypothalamus.

2. Decrease Cholesterol (And Other Testosterone Signaling Biomarkers)

Unsurprisingly, cholesterol-lowering and insulin-lowering drugs (like Metformin) have also been shown to reduce total testosterone production. While the mechanisms aren’t entirely clear, this may be due to brain signaling response changes. For instance, the hypothalamus might tell the testes to produce less testosterone if it senses we have lower levels of circulating cholesterol and insulin. And the less free testosterone we produce, the less there is to convert into DHT – the alleged “hair loss” hormone.

Note: these drugs and steroids are merely examples, and not meant to be misconstrued as the most potent free testosterone reducers, or the only free testosterone reducers.

The Problem With Suppressing Total Androgen Production? Shrunken Testicles

Unfortunately, when we mute testosterone production, we pay a steep price. When we manipulate our brain’s signaling so that our hypothalamus tells our testes to produce less testosterone… our testicles can actually start shrinking.

This is called hypogonadism – a condition that’s twice as prevalent in men taking statin (cholesterol-lowering) drugs. And if we suppress testosterone production for too long, our testicles can shrink to a size of complete dysfunction.

In a sense, this is “chemical castration” – taking testosterone-suppressing drugs at the consequence of rendering our testes lifeless…

…Which brings us to the extreme end up the spectrum: cutting off the ability for our testes to produce 95% of our body’s testosterone.

3. Reduce Testes’ Ability To Produce Androgens

In some forms, this is just the end-result of long-term testosterone-suppressing drug use. But at its very extreme, this is removal of the testicles.

Yes, I’m talking about castration. Yes, this is the ultimate DHT suppressor. And yes, this a terrible idea. If you’re looking to live a life with a near-absent libido, poor-to-no erection quality, depression, and possibly even a higher susceptibility to certain diseases and cancers – this is what life is like for some male castrates.

I don’t know about you, but I’d choose baldness over castration any day – chemically-induced or otherwise. So please, don’t get any ideas.

Summary So Far

We’ve just completed the first pillar of our flowchart… reducing DHT by reducing free testosterone.

The key takeaway: fighting DHT by reducing free testosterone is a bad idea… unless you’re decreasing DHT by increasing androgen-binding proteins like sex hormone binding globulin or albumin.

Above all: stay away from drugs that suppress total androgen production. While it’s not covered in this article, even treatments like testosterone replacement therapy can, over time, decrease your body’s ability to produce endogenous testosterone – or in other words, testosterone from the testes. The end-result? Hypogonadism. Which is ironic when you consider that both suppressing testosterone production and injecting testosterone outside the body can both result in shrunken testicles.

The good news: the next article uncovers slightly better ways of going about reducing DHT for pattern hair loss. The third article dives into some very effective topicals. And the final article uncovers DHT-fighting breakthroughs almost no one is talking about.

What’s Next…

In the next article, we’ll uncover DHT’s second “angle” of attack – reducing DHT by inhibiting the enzyme 5-alpha reductase. And if you think Propecia, Avodart, or even “natural” supplements like saw palmetto extract or pumpkin seed oil are the only ways to reduce this enzyme… think again.

Propecia And The Fear Of Sexual Side Effects

When it comes to treating hair loss, many men feel trapped between two terrible choices:

Choice #1: Start taking a drug forever that will help fight hair loss – but at the risk of developing sexual side effects (that are sometimes reported as permanent).

Choice #2: Don’t take that drug… and instead, accept that you will continue to lose your hair.

This is exactly how I felt when, at 17-years old, my doctor diagnosed me with pattern hair loss and then prescribed to me Propecia.

Propecia – an FDA-approved drug – helps slow, stop, and even partially reverse hair loss by reducing the amount of DHT in our bodies (a hormone that may trigger pattern hair loss).

Unfortunately, the hormone DHT (dihydrotestosterone) isn’t just implicated in hair loss… It’s also critical for male sexual development. In fact, men who have never been able to produce normal amounts DHT tend to suffer from low libido and poor genital development. So it’s no surprise that the drug Propecia (Finasteride) – a DHT reducer – is often maligned online as causing similar side effects: lower sex drive, poorer quality erections, and in rare cases, impotence. For an unlucky few, these sexual side effects might persist even after they stop taking the drug (although the evidence here is still debated).

As a high schooler with thinning hair, I didn’t want to risk impotence – no matter how small the chance. So I decided against taking Propecia.

But here’s something I never understood…

Many People Are Afraid To Take Finasteride To Reduce DHT, So They Instead Take “Natural” Supplements To Reduce DHT. What Difference Does It Make?

Many hair loss sufferers who fear Propecia’s sexual side effects instead take what they call “natural” DHT reducers… supplements like saw palmetto or pumpkin seed oil.

Their rationale? They say that “natural” DHT blockers reduce DHT… but without the same sexual side effects as Propecia.

At first glance, that makes no sense. Propecia, saw palmetto, and pumpkin seed oil do the same thing: they decrease DHT. But DHT is required for proper sexual development. So how come Propecia has a history of sexual side effects… while, according to some supplement advocates, “natural” DHT blockers don’t?

Or maybe these supplement takers are wrong about their “natural” DHT reducers. Maybe these supplements do cause sexual side effects, but no one has ever looked deep enough in the literature.

This article uncovers the answers. By the end, you will learn:

1. Why the word “natural” is subjective, confusing, and misleading
2. Do natural DHT blockers cause sexual side effects? The answer may surprise you
3. How natural DHT blockers may reduce DHT differently than Propecia – and how this relates to your sex drive
4. If we stop taking DHT blockers – natural or synthetic – are we worse off than if we never started?
5. Should we use natural DHT blockers to fight pattern hair loss? And if so, how?

Warning: this article gets technical. But if you’re considering taking any kind of natural DHT blocker – then you might want to read this content.

Let’s start by reviewing how DHT is connected to pattern hair loss, how reducing DHT might help fight thinning hair, and where Finasteride comes into play.

The DHT-Pattern Hair Loss Connection

When I was first diagnosed with pattern hair loss, I asked my doctor why my hair was falling out. His answer:

DHT (a hormone made from testosterone) is higher in the scalps of balding men. For reasons not entirely understood, our hair follicles start to become more sensitive to DHT, and then begin to shrink over a series of hair cycles. The end result: pattern hair loss (and eventually baldness).

Beyond this relationship, the DHT-hair loss connection is cemented by two major findings:

1. Boys who are castrated before puberty produce 95% less DHT for the rest of their lives. Interestingly, castrated prepubertal boys never go bald later in life.
2. Some men have a rare genetic mutation that prevents DHT from binding to their scalp tissues. These men also never lose their hair to pattern baldness later in life.

While researchers still can’t explain why DHT causes hair loss, the evidence is clear: (1) men who can’t produce DHT don’t go bald; and (2) balding men have elevated DHT levels in their balding regions. So goes the DHT-hair loss connection…

These findings were the basis for pharmaceutical companies to develop drugs that could reduce DHT, and hopefully reverse pattern hair loss.

Enter Propecia… A Drug That Reduces DHT

Finasteride (branded as Propecia) reduces DHT. How? By inhibiting an enzyme known as type II 5-alpha reductase.

5-Alpha Reductase, DHT & Pattern Hair Loss: What You Need To Know

Remember how DHT is made from testosterone? Well, this conversion doesn’t just happen on its own. In order for testosterone to convert into DHT, it needs the help of an enzyme called 5-alpha reductase.

5-alpha reductase is an enzyme required for our bodies to convert free (unbound) testosterone into DHT. Without 5-alpha reductase, this conversion doesn’t happen.

The 5-alpha reductase enzyme comes in a few types, but the one that is of highest interest to hair loss researchers is type II 5-alpha reductase. Why? Because type II 5-alpha reductase is the exact enzyme needed to convert testosterone into DHT in our prostate tissues and scalp skin.

Do you recall that rare genetic mutation which prevents some men from going bald? That mutation is actually a type II 5-alpha reductase deficiency. The reason why men with that mutation don’t go bald is because they don’t have any scalp DHT, and the reason why they don’t have any scalp DHT is because their bodies can’t produce the type II 5 alpha reductase enzyme.

Finasteride’s goal: to do the same thing.

Finasteride Reduces DHT By Inhibiting Type II 5-Alpha Reductase

The logic behind Finasteride is as follows: if we can stop type II 5-alpha reductase from forming, then we can stop DHT from binding to our scalps.

Finasteride (Propecia) does exactly this. It inhibits type II 5-alpha reductase, and in doing so, reduces DHT levels in our prostates, scalps, and other tissues.

Is Finasteride Effective?

Yes. While studies show that Finasteride (Propecia) isn’t great at regrowing all lost hair, the drug can significantly slow, stop, or even partially reverse the progression of pattern hair loss.

But for a select few, this may come at the cost of sexual side effects.

The Evidence: Sexual Side Effects of Finasteride

Depending on the dose, Finasteride can reduce serum levels of DHT by ~70%.

While this may help regrow hair, a DHT reduction this severe sometimes coincides with the following side effects:

• Impotence
• Depression
• Lacking sexual appetite
• Difficulty orgasming
• Low volumes of ejaculation
• Gynecomastia (or the more familiar term: man boobs)

Propecia’s manufacturers say these effects are rare and only impact up to 2% of drug users. But some studies suggests that incidence is much higher.

In one study, men taking 5mg daily of Finasteride saw a 15% incidence in sexual side effects within one year. And while this isn’t a perfect apples-to-oranges comparison (when it comes to hair loss, most Finasteride users take up to 1mg daily instead of 5mg), it’s an indicting example of how 5-alpha reductase inhibiting drugs may curb our sexual performance.

The Good News: Finasteride (Propecia) And Dutasteride Aren’t The Only Things That Can Reduce DHT

There are many foods (and food derivatives) that also reduce 5-alpha reductase activity, and thereby DHT levels.

For example, studies show that the extract from saw palmetto fruit is a 5-alpha reductase inhibitor. And some studies suggest the fatty acids in pumpkin seed oil also reduce DHT levels.

There’s also evidence that a seaweed extract called ecklonia cava may have DHT-reducing capabilities. And even the volatile oils inside rosemary and peppermint extracts show some ability to reduce 5-alpha reductase activity.

Many hair loss sufferers refer to these extracts and concentrations as “natural” DHT reducers. And as a result, most people also consider these safer.

But are these food derivatives actually safer than Finasteride? The research is more complicated than you’d expect…

And even more complicated? People’s definitions of the term, “natural”… And why, for some reason, these DHT blockers are considered “natural” while Finasteride isn’t.

DHT Reducers: Why “Natural” Is A Ridiculous Term

When we define things as natural or unnatural, what do we mean?

Some people say that “natural” is anything that can’t kill you. According to these people, substances like cyanide or arsenic are unnatural.

Unfortunately, both cyanide and arsenic are naturally-occurring substances found all over the world. And they can kill us fairly easily.

Other people loosen their definition of “natural” to anything that isn’t harmful to our health – like water. But if we think about this critically, too much of anything can harm us. In fact, too much water can kill us.

Then we’ve got a group of “natural” thinkers who are sort of scientifically literate. They say that anything made in nature = natural. Anything made in a lab = unnatural.

I decided to poll ten people who agreed with this definition. When I asked if they considered steroids unnatural, 100% said yes.

Then I explained that synthetic estrogens (a lab-made steroid) are made from concentrations of the “natural” food source wild yams. And so came another tightening of their natural definition…

My point is this: people have wildly different takes on what is natural, and what isn’t. So before you go throwing out the term, make sure you know where your definition of “natural” starts and stops.

For purposes of this article, we’re going to draw a hard line too.

“Natural” DHT Reducers: Our Definition

I think a fair definition of a “natural DHT inhibitor” is one that is…

1. Food-based
2. Chemically unaltered

For example: pumpkin seed oil and saw palmetto extract fit my definition of natural DHT inhibitors. Why?

For one, both are derived from foods. Pumpkin seed oil is made by cold pressing the seeds of pumpkins. Saw palmetto extract is made by extracting the polyphenols, phytosterols, and fatty acids from the saw palmetto fruit.

And aside from being highly concentrated, these extracts aren’t chemically altered. In other words, they’re not molecularly modified to look and act like a hormone in our bodies.

Now contrast this with Finasteride (Propecia).

Finasteride is synthetic. It’s made in a laboratory by modifying the chemical bonds of progesterone – an endogenous sex steroid released by the ovaries and the placenta during pregnancy.

And based on our research, Finasteride is not made from food. It’s a chemically altered derivative of progesterone that binds to a cofactor required for type II 5-alpha reductase expression, and as a result, stops that expression from happening.

As a result, I consider saw palmetto and pumpkin seed oil natural, and Finasteride as unnatural (at least if I had to put definitions on them).

• Natural = food-derived, chemically unaltered.
• Unnatural = not from food, chemically synthesized.

Now that we know just how pure and “natural” saw palmetto and pumpkin seed oil are, surely they must be devoid of sexual side effects… I mean, they shouldn’t boast any sexual problems like the “unnatural” drug Finasteride… Right?

Wrong. (Sort of).

The Evidence: Sexual Side Effects of “Natural” DHT Inhibitors For Hair Loss

Saw Palmetto

While the evidence is mixed, there are some reports that saw palmetto is sometimes associated with sexual dysfunction such as decreased libido.

The good news? These side effects seem less common with saw palmetto versus Finasteride. Moreover, the adverse effects of saw palmetto (if any) appear to be mild and infrequent. Lastly, a recent large multi-center study found no evidence of significant adverse effects (including sexual dysfunction) after 18 months of treatment with saw palmetto… at three times the typical dose.

We can’t say the same about mega-dosing with Finasteride, as that earlier study showed that 5mg daily dose resulted in a 15% incidence of male sexual side effects in just one year. At the same time, I’m making a crude apples-to-oranges comparison. If we really wanted to answer this question, we’d need to compare Finasteride against saw palmetto within the same clinical trial… and ask the participants detailed questions about rates of sexual side effects.

That research currently doesn’t exist. So we’re left drawing crude comparisons and taking our best guesses.

The bottom line: there’s some evidence that saw palmetto may cause some sexual side effects. But these effects are probably much milder versus Finasteride.

So, what about other “natural” DHT reducers – like pumpkin seed oil?

Pumpkin Seed Oil And Other “Natural” DHT Reducers: Any Sexual Side Effects?

There are reports that pumpkin seed oil may cause ejaculation problems. However, several recent studies on patients receiving pumpkin seed oil over 6-12 months have shown no significant sexual side effects.

We also haven’t observed any sexual side effects with topical rosemary oil use – another anti-androgenic extract. And ironically, the seaweed extract ecklonia cava may reduce DHT levels in men while simultaneously improving their sexual function.

The Takeaway: Natural 5-Alpha Reductase Inhibitors Reduce DHT, And Probably With Fewer Sexual Side Effects Than Propecia

And this brings us back to our main question…

How can both natural 5-alpha reductase inhibitors and Finasteride reduce DHT… but only Finasteride is associated with higher rates of sexual dysfunction?

There are at least four possibilities.

Hypothesis #1: Natural DHT Blockers Don’t Cause Side Effects, Because People Don’t Perceive They Should Cause Side Effects

This is called the nocebo effect, and it happens all the time in research.

For example, one study on Finasteride showed that simply by warning patients of the potential for side effects, reports of side effects rose by over 500%. The implication? Maybe many of the side effects reported by Finasteride users are psychosomatic.

When we follow this logic further, things get even more interesting. For instance, the effects of certain drugs – both positive and negative – seems to vary by cultural group. For instance, while saw palmetto is sometimes associated with sexual side effects in the U.S., it was also celebrated as an aphrodisiac for some indigenous groups.

Same plant, same ingredients, but two opposing effects.

Moreover, some studies on minoxidil have shown that men have regrown significant amounts of hair… in the placebo group! Similarly, studies on finasteride have shown men have lowered their DHT levels… by taking sugar pills!

The mind is a powerful thing.

So, maybe these “natural” DHT reducers don’t cause nearly as many side effects… simply because we don’t think they should.

Hypothesis #2: Natural DHT Blockers May Cause Sexual Side Effects, But We Don’t Yet Have The Studies To Prove It

There are an overwhelming number of studies on Finasteride and its sexual side effects. On the contrary, there are fewer studies on saw palmetto, pumpkin seed oil, and other natural DHT reducers. By volume alone, the literature skews heavily against Finasteride. As a result, we might be making misleading conclusions about these “natural” DHT reducers.

But for a moment, let’s assume this isn’t true.

Instead, let’s take the current body of evidence at face value: despite the fact that Propecia and food-based extracts reduce DHT, Propecia causes significantly more sexual side effects than saw palmetto or pumpkin seed oil.

The question is… why?

Well, there are two remaining possibilities.

First, that natural DHT reducers aren’t as effective at reducing DHT as a drug like Propecia, and as a result, produce fewer sexual problems.

And secondly, that natural DHT blockers reduce DHT through a completely different set of mechanisms, and that only certain DHT-reducing mechanisms are to blame for Finasteride’s negative side effects

Let’s take these one-by-one.

Hypothesis #3: Natural DHT Blockers are Worse at Reducing DHT than Finasteride, And Thus Cause Fewer Sexual Side Effects

This is an uncomfortable truth for most “natural” DHT reducer advocates: these natural compounds are probably less effective at reducing DHT versus Finasteride.

Finasteride And Dutasteride Drastically Reduce Serum, Prostate, And Scalp DHT

Studies have shown that Finasteride decreases serum DHT levels by 71% after 24 weeks of use. Similarly, Dutasteride has been shown to lower serum DHT by 95 % after 24 weeks.

Finasteride and Dutasteride also reduce scalp DHT by 64% and 51%, respectively. Finasteride reduces prostatic DHT levels by 85%, and Dutasteride reduces prostatic DHT levels by 97% over 6-10 weeks.

Those are some serious reductions. So how do food-based 5-alpha reductase inhibitors compare?

Sadly, we don’t really know. But based on the evidence so far, these food-based DHT reducers are much less effective.

Natural DHT Reducers Only Reduce DHT By A Fraction Of Finasteride

In a randomized trial, saw palmetto reduced prostate tissue DHT levels by 32%.

Another study showed that saw palmetto inhibits the activity of type II 5-alpha reductase by 76%, and Finasteride by 82%. Unfortunately, there was no evaluation in actual DHT levels. And to make matters worse, when we compare half-lives and metabolism rates of saw palmetto versus Finasteride, the 5-alpha reductase reduction from saw palmetto appears much shorter-lived.

Even worse news: there are no studies evaluating “natural” DHT blockers and their reduction in DHT levels in the prostate or scalp. And when it comes to pattern hair loss, the scalp is where DHT reduction really counts.

Based on the limited evidence – if we control for dosage sizes, half-lives, and the studies above – our best guess is that natural DHT blockers reduce DHT levels by just 1/3^rd of what a synthetic DHT blocker can achieve.

This would also explain why saw palmetto isn’t as effective as finasteride: it’s just not as powerful.

The take home note? With less of a reduction in DHT, fewer sexual side effects will arise. So it’s no wonder that food-based DHT reducers are associated with fewer sexual problems.

But this might not be the “big” reason why natural DHT reducers boast fewer sexual side effects. In fact, it might be due to the actual structure of these synthetically-made drugs.

Hypothesis #4: Natural DHT Blockers Indirectly Reduce 5-Alpha Reductase, Whereas Finasteride Directly Reduces 5-Alpha Reductase… Which May Explain Why Finasteride Has More Sexual Side Effects

5-Alpha Reductase Inhibitors: Steroidal Versus Non-Steroidal

Remember how we defined “natural” versus “unnatural”? Natural is food-based and chemically unaltered; unnatural is not from food and chemically synthesized.

Well, chemists also divide 5-alpha reductase inhibitors into two categories:

1. Steroidal 5-AR Inhibitors: 5-alpha reductase inhibitors made from steroids
2. Non-steroidal 5-AR Inhibitors: 5-alpha reductase inhibitors not made from steroids

Examples of steroidal 5-AR inhibitors: Finasteride and Dutasteride. Why? Because these drugs are chemically synthesized from the sex steroid progesterone.

Examples of non-steroidal 5-AR inhibitors: saw palmetto extract and pumpkin seed oil. Why? Because these compounds are simply food concentrations.

Why The Difference Between Steroidal And Non-Steroidal 5-AR Inhibitors Matters

Interestingly, steroidal 5-alpha reductase inhibitors may reduce DHT differently than non-steroidal 5-alpha reductase inhibitors.

Steroidal 5-AR Inhibitors Directly Reduce 5-Alpha Reductase

Remember our chart from earlier? Free testosterone is converted into DHT by the enzyme 5-alpha reductase…

But in reality, this process isn’t that straightforward.

Why? Because 5-alpha reductase doesn’t just pop up out of nowhere. It actually needs the help of a cofactor to form and mediate the DHT conversion process. And what is that cofactor? A coenzyme known as nicotinamide adenine dinucleotide phosphate… or to put it simply, NADPH.

Finasteride works on a molecular level by binding to and altering the structure of NADPH. It changes NADPH it into a different cofactor – one that doesn’t allow 5-alpha reductase to form.

The end-result: a direct decrease in 5-alpha reductase expression.

This is an example of direct 5-alpha reductase inhibition. And based on the evidence, this is exclusively how steroidal 5-AR inhibitors reduce DHT.

But non-steroidal 5-AR inhibitors behave differently in the body. And these differences might explain the lacking sexual side effects.

Non-Steroidal 5-Alpha Reductase Inhibitors – How Are They Different?

Before we go any further – let’s be clear: non-steroidal 5-AR inhibitors like saw palmetto, pumpkin seed oil, rosemary extract, and ecklonia cava still directly reduce 5-alpha reductase.

For example…

Non-Steroidal 5-AR Inhibitors: Direct Mechanisms

Pumpkin seed oil is high in polyunsaturated fatty acids (linoleic acid) and zinc. And interestingly, linoleic acid and zinc are non-steroidal elements which directly inhibit 5-alpha reductase. Here’s how:

Linoleic acid reduces 5-alpha reductase by altering the lipid bilayer in cell membranes. Conversely, zinc inhibits 5-alpha reductase by decreasing the expression of NADPH – the same cofactor needed for 5-alpha reductase to form.

These non-steroidal elements direct reduce 5-alpha reductase (5-AR). Why? Because they act on a molecular level to directly shut down 5-AR activity.

We see these same direct mechanisms are play with other natural DHT reducers – like saw palmetto and rosemary oil.

Saw palmetto extract inhibits 5-alpha reductase directly by competing with free testosterone to bind to androgen receptors. The more saw palmetto present, the less free testosterone can be converted to DHT. And just like saw palmetto, rosemary oil also appears inhibit 5-alpha reductase through direct actions on cell function.

But this isn’t the only way non-steroidal compounds reduce DHT levels. In fact, they also act on DHT indirectly… And evidence suggests that this type of DHT reduction – indirect – is probably much safer when it comes to sexual side effects.

Non-Steroidal 5-AR Inhibitors & Indirect DHT Reduction

Unlike Finasteride, non-steroidal 5-AR inhibitors like saw palmetto and pumpkin seed oil reduce DHT through both direct and indirect means.

As a refresher:

1. Direct – inhibit 5-alpha reductase directly (suppress 5-AR expression at molecular level).
   1. Steroidal examples: Finasteride alters the chemical structure of NADPH so 5-alpha reductase cannot form
   2. Non-steroidal examples: linoleic acid alters lipid bilayers so 5-alpha reductase cannot form; zinc decreases NADPH so 5-AR cannot form
2. Indirect – inhibit 5-alpha reductase indirectly (by reducing inflammation)
   1. Steroidal examples: none.
   2. Non-steroidal examples: compounds in saw palmetto, pumpkin seed oil, and rosemary oil help reduce chronic inflammation, and as a consequence, reduce the amount of DHT in inflamed tissues

The definition of Indirect DHT Reduction is important – so let’s reinforce it.

Indirect DHT Reduction = Reducing Inflammation

When it comes to the causes of pattern hair loss, one question worth asking is…

If DHT levels are higher in balding scalps, then what causes DHT to rise in the first place?

Doctors have a simple answer for this: genetics. But the full story is a lot more complicated. For example, DHT may not just increase out of genetic sensitivity; DHT may increase, in part, as a response to chronic inflammation.

It’s far more likely that elevated scalp DHT in isn’t just due to genetic sensitivity, but rather, that this DHT is a response to inflammation in men’s scalp skin.

The causes of scalp inflammation are still debated, as is inflammation’s role in pattern hair loss. But one thing is clear: where there’s chronic inflammation, there’s also often an increase to DHT levels.

The net: higher DHT levels are a response to chronic inflammation. And if we take away the inflammation, we may indirectly take away some DHT.

And that is how we might indirectly reduce DHT levels. We take away the sources of inflammation.

Interestingly, non-steroidal 5-alpha reductase inhibitors might partially do this…

Examples Of Indirect DHT Reduction: Non-Steroidal 5-Alpha Reductase Inhibitors

There are hundreds of studies showing how substances inside pumpkin seed oil, saw palmetto, rosemary, and ecklonia cava can reduce inflammation (and thereby DHT levels).

Covering all of them would turn this 5,000-word article in 100,000. So instead, we’ll just give a highlight reel.

Indirect DHT Reducing Mechanisms Of Non-Steroidal 5-AR Inhibitors

The following parts of pumpkin seed oil help reduce chronic inflammation:

1. Pumpkin Seed Oil
   1. Antioxidants (tocopherols): decrease oxidation, decrease expression of transforming growth factor beta
   2. Linoleic acid: reduces COX-2 enzyme
2. Rosemary Oil
   1. Polyphenols: reduce COX-2 enzyme
   2. Volatile oils: reduce COX-2 enzyme, pro-inflammatory interleukins, and tumor necrosis factor

This list could go on for pages. But you get the idea: natural DHT reducers don’t just reduce 5-alpha reductase… They also reduce the signaling proteins and enzymes that are linked to chronic inflammation in our scalp tissues. As a result, they directly reduce inflammation, and thereby indirectly reduce DHT levels.

And that might be the difference between Finasteride and natural DHT reducers: one does more to directly reduce DHT levels; the other does more to indirectly reduce them. This, maybe the natural DHT reducers cause fewer sexual side effects… simply because these compounds are indirectly reducing DHT by lowering inflammation.

Again, these are just hypotheses. Nobody really knows.

Are There Hidden Costs Of Finasteride? A Note On Dependency And Potentially Irreversible Remodeling Of Androgen Receptors

When it comes to Finasteride, there is one study that has (slightly) worried me, and that I can’t fully explain.

Finasteride, when combined with Letrozole (a drug that lowers estrogen levels), appears to increase androgen receptor activity in the prostate of gerbils. That’s not necessarily a big deal… but it’s also not the whole story. In that study, the change in androgen receptor activity didn’t go away… even after stopping Finasteride + Letrozole treatment.

Why is this a problem? Well, if this research translates to humans, that would imply that when you get off Finasteride (Propecia), your prostate may have remodeled to have an even higher amount of androgen receptors. DHT has a higher affinity for androgen receptors than many other testosterone derivatives. Because of this, there’s a chance that if you increase your androgen receptors, the more likely DHT will arrive to those sites.

In other words, if your prostate remodels and you get off Finasteride, your prostate is likely going to flood with more DHT than if you never took Finasteride to start. This may, in part, explain things like the development of androgen-independent prostate cancer.

Does Androgen Receptor Remodeling And DHT Flooding Carry Over Into Pattern Hair Loss?

We don’t know, but hypothetically it’s possible. Maybe it’s even plausible.

In fact, this would explain why men lose hair so rapidly after dropping Propecia. More DHT floods the scalp and the hair rapidly miniaturizes… potentially sending people lower than their baseline (i.e., had they never started treatment in the first place).

Again, we just don’t know if these findings in gerbil prostates apply to humans with pattern hair loss, or if androgen remodeling with Finasteride + Letrozole is similar to that which  might occur with Finasteride alone. Moreover, those gerbils were taking 10mg/kg of Finasteride – the equivalent of 720mg of Finasteride daily for humans. That feels like a supraphysiological amount for humans, and so it’s very possible that these study results do not apply to humans.

In any case, they do warrant more investigation, and maybe slightly more cause for concern among people considering the drug.

Do “Natural” DHT Blockers Like Saw Palmetto Or Pumpkin Seed Oil Remodel Androgen Receptors?

The answer to this question is that we don’t know.

While saw palmetto has been shown to not influence androgen receptor activity, there are no other studies (to my knowledge) that have evaluated this issue. But what’s assuring is that food-based DHT blockers…

1. Are less potent than Finasteride, and…
2. Seem to reduce DHT through direct and indirect means

Both of these likely lower the risk of irreversible tissue remodeling.

Moreover, natural DHT reducers have other health benefits besides promoting hair growth – like reducing oxidation and chronic inflammation – processes not only detrimental to our hair, but to our entire body. And if you’ve been keeping up with these articles, you’ll know how just how closely these processes are associated with nearly all disease development.

Should You Include “Natural” DHT Reducers In Your Hair Loss Regimen?

They’re not very effective. But if going all-natural is very important to you, than you can certainly try them.

Based on the evidence, “natural” DHT blockers – saw palmetto, pumpkin seed oil, rosemary oil, and ecklonia cava – seem to be somewhat effective at reducing DHT. They’re also derived from food substances as opposed to chemically altered steroids – which might make them safer (again, we just don’t know for sure).

For instance, drugs like Propecia appear to have no other benefits to cardiovascular health or longevity. Conversely, studies show that the substances inside “natural” DHT reducers may have anti-inflammatory properties that confer to longer-term health benefits: a reduction of reactive oxygen species, lower levels of inflammation, and more.

Final Thoughts

You have hundreds of “natural” DHT reducing supplements from which to choose. So, which are the best? We don’t yet know. What we do know is that these things aren’t as powerful as Finasteride… at least in their current formulations.

You could try saw palmetto, pumpkin seed oil, rosemary extract, peppermint oil, castor oil, olive oil, and just about every essential oil out there. All of these appear to have some anti-androgenic effects. At the same time, just because something is natural doesn’t make it safe.

If you do decide to try a “natural” DHT reducer – commit to it for at least six months before determining if it’s helping your hair loss. Better yet, do it in conjunction with mechanical stimulation exercises. Chances are the two will create a synergistic hair regrowth effect (read the case study in our saw palmetto article).

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

Read Time: 10 minutes

Will These Topicals Reverse Your Hair Loss?

People often ask me if a new topical mentioned by a doctor, website, or hair loss forum will help regrow their hair. Here’s a running list from my emails just last week:

• Emu oil
• Argan oil
• Castor oil
• Coconut oil
• Onion juice
• Shea butter
• Egg yolk
• Rogaine

In the last decade, if there’s anything I’ve learned about topicals, it’s this: topicals are a shot in the dark.

What works for one person does not work for 99% of others. I’ve experimented with almost all of the above topicals, and for months at a time. None of them helped regrow my hair.

With that said, my story isn’t everyone’s story. Sometimes people get lucky. Sometimes a person uncovers a topical that gives them significant regrowth.

But why is that? How can one topical regrow hair for one person but not for everyone else?

That’s what this article is about.

Why Most Topicals Fail To Regrow Any Hair

Reason #1 – Genes & Gene Expression

It’s been well-established that our genes predispose us to hair loss. For instance, if we have this genotype, we’re twice as likely to go bald. If we have this genotype, we’re seven times more likely to bald. (Note: “predisposed” does not mean “destined”.)

Interestingly, our genes and gene expression also influence how well we respond to hair loss drugs.

Studies show that Propecia is more effective for those with certain gene variants (polymorphisms). For reasons not yet understood, people who have these polymorphisms and take Propecia tend to recover more hair than those without them.

We can apply that same logic to any hair loss topical – like Rogaine.

Rogaine’s mechanisms are mysterious, but most experts agree that Rogaine helps boost blood flow to hair follicles – in addition to modulating prostaglandin activity in epithelial and dermal papillae cell sites. However, the magnitude of effect that Rogaine will have probably depends on a person’s…

• Sensitivity to minoxidil (the active ingredient in Rogaine)
• Skin permeability (the higher Rogaine’s penetration, the better the hair recovery)
• Sulfotransferase activity (the enzyme that “turns on” minoxidil in the scalp)
• Gene variants that might help regulate blood pressure, potassium ion channels, or even collagen remodeling

All of these markers link back to our genes (and gene expression). Genetics likely explains why some men and women using Rogaine regrow some hair, while others (like myself) see no changes at all.

But this is just one reason. That’s not all that’s going on.

Reason #2 – Your Topical Might Not Target Why You Personally Are Losing Your Hair

There are a million different reasons why someone starts losing their hair. Telogen effluvium-related hair shedding is linked to stress, nutrient imbalances, and chronic conditions like hypothyroidism or heavy metal toxicities. Pattern hair loss is linked to increased scalp DHT. And for pattern hair loss sufferers – there’s also a gradient of involvement of scalp DHT. Some DHT arrives to the scalp by favoring the 5-alpha reductase pathway; some DHT might favor alternative pathways – thus making 5-alpha reductase inhibiting drugs less effective.

Unfortunately, most hair loss topicals target just one or two “targets” of the myriad possibilities for why you might be losing hair.

• Spironolactone – blocks androgen receptors (potentially great for female pattern hair loss)
• Finasteride – inhibits 5-alpha reductase (potentially great for androgenic alopecia)
• Rogaine – increases blood flow, modulates prostaglandins (potentially great in the medium-term for many hair loss types)
• Onion juice – reduces inflammation (potentially great for alopecia areata, much less so androgenic alopecia)
• Apple polyphenols – decreases transforming growth factor beta (potentially great for inflammatory-related hair loss disorders, though evidence is incredibly limited)
• Nizoral – anti-fungal, maybe decreases DHT (potentially great for telogen effluvium and androgenic alopecia)

So, without guidance, how likely is it that we pick a topical that also happens to target the same triggers of our own hair loss?

Not very likely. And when you factor in other issues for less-studied substances – i.e., half lives of ingredients – things become even more convoluted.

This sort of thing happens in hair loss forums all the time. Here are two examples.

Topical Study #1: Pig Lard

In September 2013, a researcher published a paper about how he used a pig fat (lard) topical for his own personal hair regrowth. This researcher massaged five grams of fat (lard) into his scalp each night before going to bed. After eight months, he’d regrown a ton of hair:

(source)

This study got posted on hair loss forums, and within days, its popularity exploded. Dozens of forum users decided to commit to the methodology for eight months and try to validate its results.

So what happened?

After a month people’s excitement started to sizzle. After two months the thread got buried to the forum’s second page. After three months people forgot the study had ever been posted. And after eight months none of the “testers” posted a single before-after picture. Of the testers who finished the experiment (to my knowledge – just two), none claimed any results.

This story isn’t unique. This is the typical trend with any treatment on any hair loss forum:

1. One treatment success story
2. Initial excitement from the community
3. A few users who say they’re going to try it themselves
4. No updates from those users
5. A slow fade into radio silence

For purposes of this article, let’s assume that of the testers who tried this topical, they tried it correctly and for the entire eight months, and it still didn’t work. Let’s forget about the possibility that most testers who faded away probably didn’t even commit to the regimen (which is probably the reality).

Why would this lard topical work for the author but not everyone else? Well, there are a variety of possibilities:

• Product quality variances (perhaps pig lard’s fatty acid composition varies greatly depending on preparation methods)
• Half-life limitations (perhaps pig lard is only effective if you can use it several times per day)
• Differing hair loss types (perhaps this individual case was dealing with a unique subset of androgenic alopecia)

Topical Study #2: Essential Oils

Many years ago researchers conducted a study on aromatherapy essential oils’ effects on hair growth for people with Alopecia Areata.

Alopecia Areata is an autoimmune disease in which the body attacks the hair follicle, often leading to hair fall in patches and everywhere (even on the scalp sides).

The researchers tested a cocktail of thyme, rosemary, lavender, and cedarwood essential oils inside a mixture of jojoba and grapeseed. The instruction: massage these oils into the scalp, daily, for 2+ minutes.

The results were incredible.

44% of users saw hair improvement. Some even saw full recoveries:

(source)

Again, this study made its rounds through hair loss forums. People got excited. Many pattern hair loss sufferers said they would attempt to replicate the study and try it themselves.

Months later those threads went quiet. We never saw any before-after photos from those who said they’d commit to the regimen.

Why did this essential oil topical work for those in the study and not for the forum testers?

Why Essential Oils Don’t Regrow Hair For Everyone

This one is kind of obvious. The study was for people with alopecia areata – not male pattern hair loss.

Alopecia areata is an autoimmune disease where the body begins recognizing hair follicles as invaders, and then begins to attack and destroy them.

Those with alopecia areata don’t necessarily have any of the scalp conditions associated with male pattern baldness (calcification, fibrosis, higher tissue DHT, etc.).

As such, alopecia areata sufferers and male pattern hair loss sufferers responder better to different types of treatment.

Advice For Alopecia Areata Sufferers

If you’re suffering from alopecia areata, this topical might be worth trying. But only if other frontline therapeutics for alopecia areata have already failed you. If you’re suffering from regular pattern hair loss, don’t expect an essential oil blend to work any miracles.

Final Thoughts On Hair Loss Topicals

Prioritize topicals that rank highest in terms of Evidence Quality and Regrowth Potential. Deprioritize topicals with ingredients that are poorly supported, at least until enough data comes out to revise your opinions.

If you’re going to try a topical, do the following:

• Test it for at least six months before deciding whether it’s helpful. In cases of finasteride, results often won’t peak for 18-24 months.
• Don’t change a dozen other things in your regimen at the same time, at least if your exclusive goal is to judge the standalone efficacy of that topical.

Otherwise, you won’t have any idea what’s helping.

Read time: 15 minutes

What Causes Hair Loss?

If you ever google’d “what causes hair loss?”, you’ll find thousands of results saying hair loss is due to…

• Genetics
• DHT (dihydrotestosterone)
• High testosterone

…and a million other one-liner answers.

The reality? These statements are too simple to be right or wrong. For instance:

Yes, our genes might predispose us to hair loss, but gene expression likely matters more than genes alone.

Yes, DHT (a hormone made from testosterone) is linked to hair loss… But only one kind of DHT: scalp tissue DHT. Paradoxically, serum (blood) DHT is sometimes linked to lower levels of scalp hair loss, and body tissue DHT encourages body hair growth.

Yes, hair loss occurs in high-testosterone men… But it also occurs in low-testosterone men. What actually matters is the amount of testosterone converting into scalp tissue DHT – and why.

So how do we distinguish hair loss fact from fiction? As one reader recently wrote in…

“I have been losing my hair for about ten years and I don’t really know where to start because of the overload of information online. What do you recommend are the first steps I can take?”

Unfortunately, there’s no easy answer. So my #1 recommendation is: get informed.

Learn Everything You Can About Hair Loss Science

Don’t just read summary articles. Read peer-reviewed studies. And don’t just read abstracts. Read full papers. Don’t know a term? Look it up. Have a question? Email the author. You’d be surprised how many will get back to you.

The more you know, the better informed you are, the quicker you can sort out the misinformation.

Of course, not everyone can spend years of their life reading pubmed journals. And not everyone can access the full texts from studies. That’s why  I wrote this article – to share some of my ideas on hair loss pathology, formulated over the years.

Inside This Article: The Causes Of Hair Loss Mapped Into A Flowchart

This a long post. The goals are to simplify some elements of hair loss science so we can better understand the benefits (and limitations) of treatments, as well as some angles of attack for pattern hair loss. If you have any questions, please reach out in the comments.

Important Note: since writing article, my views on pattern hair loss have evolved. While the following article helps to clarify two rate-limiting recovery factors in pattern hair loss, it fails to dive deep enough into the genetic predisposition of AGA, its potential relationship to mechanotransduction, a concrete explanation for the DHT paradox, and a rationale for the patterning of hair thinning in men and women.

Rather than continuously revise this article and distill what is (very) complex science into lay terms, I instead decided to write a manuscript and submit these ideas to peer-review. The paper was accepted in late 2017. You can read it in full right here, along with a lay person’s breakdown of (some of) its arguments here.

Otherwise, please consider this article a starting point to uncovering additional factors (beyond DHT) involved in androgenic alopecia. And, please disregard my original emphasis on diet, lifestyle, and testosterone:estrogen ratios. While these factors are certainly linked to systemic inflammation and non-androgenic forms of hair loss, the sources of inflammation in AGA are a little less clear, and likely less connected to these factors than I originally implied.

Finally, here is a more updated overview: Androgenic alopecia: its causes, treatments, and unknowns.

Tracing The Causes Of Hair Loss: Where To Begin?

Let’s start with what our fingers feel and our eyes see: our thinning hair and the skin underneath it.

A Close-Up Of The Balding Scalp

Where is your hair thinning? Temples? Vertex? All over? Using your hands, feel the thinning areas of your scalp. Then feel your non-thinning areas (the sides or back of your head).

Notice anything? In balding sites, our skin feels thicker, less pliable, and significantly less elastic. Touch the green part of your scalp, then the blue. Feel the difference.

Balding Regions Have Thicker, Tighter Skin

Next, grab a mirror and look at your head. Do you see any visual differences in your balding versus non-balding regions?

In balding areas, many men’s scalps have a certain “shine” to them. You might see this too. In advanced stages, some balding regions can even look swollen.

Balding Regions Are Shinier, More Swollen

Why do balding parts of the scalp feel tighter, thicker, and look shinier and more swollen?

Your balding scalp is tighter, thicker, and shinier because of an overproduction of something called collagen.

Collagen is the fibrous protein that makes up our connective tissues, like our skin. If you ever get a small paper cut, your skin cells make new collagen to repair the wound and make the skin as smooth as it used to be. But if we cut our skin too deeply, our skin can make too much collagen.

But it’s not just too much collagen. It’s disorganized collagen cross-hatchings. This leads to imperfect healing and scar tissue.

Balding Skin Is Tighter, Thicker, And Shinier Due To Excess (Disorganized) Collagen

Interestingly, men with pattern hair loss have four times the amount of collagen fibers at the temples and vertex than men with no hair loss at all. What does that indicate? Balding skin is ridden with scar tissue.

Disorganized (Excess) Collagen Is Also Called Fibrosis

There’s another word to describe the disorganized, over-accumulation of collagen: fibrosis. And while our balding scalps are wrought with excess collagen, our thinning follicles are also surrounded by it! This is called perifollicular fibrosis.

In other words… where there’s hair loss, there’s fibrosis. But does fibrosis cause hair loss?

We can find our answer by studying a rare autoimmune condition that makes people over accumulate collagen and fibrosis. It’s called scleroderma.

The Scleroderma-Fibrosis-Hair Loss Connection

In scleroderma, the body starts to overproduce collagen – sometimes in the lungs, hands, and even the scalp. Regardless of the location, this process results in the same visual symptoms we see in balding scalps: tighter, thicker, shinier-looking skin.

Just look at this photo of a scleroderma sufferers’ hands, and then this photo of a hair transplant patient’s scalp.

Notice the shine around the knuckles and the shine across the top of the scalp… It’s the same skin quality. Same shine, same thickening, same swelling.

But most interestingly, for those who develop scleroderma in the scalp, hair loss soon follows.

That’s a critical piece of information. It confirms that excess collagen and fibrosis occur before hair loss starts. They precede hair thinning. Excess collagen and fibrosis accumulate first, then hair loss comes later.

Scalp Fibrosis Develops Before Hair Loss

Knowing this, we can begin to build our flowchart:

But how exactly does disorganized, excess collagen (or fibrosis) lead to hair loss?

Fibrosis Restricts Blood Flow To Our Hair Follicles

Body tissues wrought with excess collagen and fibrosis also have lower blood flow. This is even documented in balding regions – blood flow is restricted in thinning areas of our scalps. The more collagen and fibrosis, the more blood flow is restricted.

Knowing this, it’s no surprise that nearly all scleroderma sufferers also have poor circulation of the extremities (hands, feet, and head). Poorer circulation, less blood flow… But less blood flow also means less oxygen.

Lower Blood Flow Lowers Your Tissue’s Oxygen Supply

Blood carries oxygen to our tissues. If our tissues have lower blood flow, they also have lower oxygen levels. Low tissue oxygen is also known as hypoxia. Studies confirm that balding scalp regions are hypoxic.

If a tissue is chronically suffering from low blood flow and low oxygen, hair cannot grow.

In one study, men’s balding regions had just 60% the oxygen levels of non-balding areas. Men with no hair loss had oxygen levels nearly the same all across their entire scalp.

Knowing this, we’ve just added to our flowchart. Excess collagen (fibrosis) decreases blood flow and oxygen, and in doing so, “chokes out” our hair follicles. This leads to hair loss.

Now, are there any other conditions in a balding scalp that might also decrease blood flow and thereby oxygen to our follicles?

Yes. Beneath our scalp skin is another contributing factor: arterial calcification.

Our Scalps Have Become Partially Calcified

It’s not just fibrosis that reduces blood flow and oxygen to our hair. In balding areas, the blood vessels that indirectly support our follicles – in the lower layers of the scalp – may have also become calcified!

Dr. Frederick Hoelzel in the American Medical Association published the connection between scalp calcification, restricted blood flow, and hair loss over 70 years ago. When removing the brains of cadavers, he discovered:

“Baldness occurred in persons in whom calcification of the skull bones apparently had not only firmly knitted the cranial sutures but also closed or narrowed various small foramens through which blood vessels pass most prominently in persons with a luxuriant crop of hair.”

For the layperson – in balding regions, our scalp bones and blood vessels supporting the follicles are calcified. If an artery is calcified, blood flow is significantly restricted.

What Is Calcification?

According to medical experts, calcification is “when calcium builds up in places where it doesn’t usually appear, like the coronary arteries or brain.”

Since elderly people often have more calcification, researchers once thought this process was a part of normal aging. But it turns out the relationship between age and calcification doesn’t really exist. Calcification doesn’t have to increase with age. It can be rampant in young adults and nearly absent in older ones.

And finally, it’s also important to note that calcification is not necessarily caused by a calcium-rich diet.

So back to our flowchart. Does calcification cause fibrosis?

Probably not. Most research suggests that calcification and fibrosis can occur in the same areas, but are likely independent of each other. And while some scleroderma patients also suffer from soft tissue calcification, others just suffer from an overproduction of collagen. So calcification does not have to happen before fibrosis and vice-versa.

Knowing this, we’re ready to add calcification into our flowchart. For simplicity’s sake, we’ll remove the visuals describing a balding scalp – the “thicker, tighter, shinier skin.”

Now let’s start tracing this chart backwards. We’ve gone as far as calcification and fibrosis. So what triggers both?

Calcification And Fibrosis Precede Hair Loss…

…But What Causes Calcification And Fibrosis?

We can get an idea of what might be causing these conditions if we look at the people most likely to develop arterial calcification and fibrosis: men.

Men are almost twice as likely as women to develop calcified arterial lesions. Why is that? Researchers have long suspected that androgens might be to blame. Read: testosterone and DHT – or dihydrotestosterone.

Why is this so interesting?

Well, most doctors agree that DHT causes hair loss… But none actually know how DHT causes hair loss. If DHT triggers calcification and fibrosis, this explains how DHT causes hair loss. But to confirm this, we need to know if androgens (like DHT) actually precede arterial calcification and fibrosis.

The DHT-Calcification-Fibrosis Connection

Does DHT Cause Calcification And Fibrosis?

Research here is mixed.

On the one hand, men and women who take androgens (steroids) significantly increase their risk of arterial calcification. And in mice, DHT and testosterone injections increase arterial calcification lesions by 200-400%. The more DHT or testosterone injected, the greater the calcification. That’s a pretty strong case that androgens cause calcification.

But paradoxically, in studies done in test tubes (outside of our bodies), increased androgens don’t cause calcification. In these tests, androgens protect against calcification.

This suggests two things:

1. Androgens alone don’t cause calcification
2. The test tube studies are missing at least one variable. It must be that increased androgens plus at least one “mystery variable” leads to calcification – but not androgens by themselves.

DHT is the main androgen associated with pattern hair loss. But we also know that DHT alone doesn’t cause calcification and fibrosis… So DHT by itself can’t be the problem.

What does this suggest?

In the scalp, increased DHT plus these “mystery variables” precede both calcification and fibrosis. Knowing this, here’s our new flowchart:

So what could these mystery variables be?

Well, there are two. The first is an increase in androgen receptors. The second is an imbalance of calcification regulators. And explaining both are a bit of a mouthful. So bear with me.

A Crash Course On DHT, Androgen Receptors, And Calcification Regulators

We know that androgens alone don’t cause calcification, and that in the body, androgens must be interacting with other variables to cause calcification and fibrosis. So, what are those variables?

It appears there are two. And in 2016, researchers finally confirmed the first one: androgen receptors.

What Is An Androgen Receptor?

An androgen receptor (AR) is the place inside a cell where androgens – like testosterone and DHT – attach themselves. Think of an androgen receptor (AR) like the landing pad for DHT. Without its landing pad, DHT doesn’t bind to the cell.

Here’s a visual. This is a cell, and the yellow puzzle pieces (labeled AR) are androgen receptors:

(source)

Androgen receptors aren’t always active. They typically turn on in the presence of DHT or testosterone, then turn off when these hormones aren’t around.

The Connection Between Increased DHT And Increased Androgen Receptors

In our scalp tissues, increased androgens turn on more androgen receptors, and together, the increased DHT plus the increased androgen receptors results in calcification. Both DHT and androgen receptors must increase (not just one) for calcification to occur.

 Interestingly, DHT plus androgen receptors also increase fibrosis in heart cells.

In other words, increased DHT + increased androgen receptors precede both calcification and fibrosis.

But here’s where things get tricky… Increased androgen receptors aren’t the only other variable. We know this because of DHT’s biggest paradox:

Increased tissue DHT encourages hair loss in the scalp, but encourages hair growth in the face and body.

That means that in our hairy facial and body tissues, calcification and fibrosis don’t occur. Why? Because in our bodies and face, increased DHT instead encourages hair growth – just the opposite of our scalps.

If our flowchart is accurate, this means that in the body and face, when DHT increases, androgen receptors must not increase. Otherwise, our body and facial tissues would also calcify, and hair wouldn’t grow.

But as it turns out, both balding scalps and hair-bearing body and facial tissues have increased DHT and increased androgen receptors… Yet hairy body and facial parts aren’t calcified or filled with fibrosis.

What does all of this mean?

In addition to DHT and androgen receptors, another factor must also be causing calcification and fibrosis. Either something is protecting our body and face from fibrosis and calcification, or something is causing both to happen in our scalps.

Taking this into account, here’s our new flowchart:

So, what is this new mystery variable? There are several contenders, but diving into all of them would turn this already-monstrous post into a full-blown book.

The reality is, we don’t yet know for sure.

The reason why: 99% of researchers still abide to the DHT-sensitivity argument. They say that “genetics” makes our hair follicles more sensitive to DHT, and that for unknown reasons, DHT accumulates in the scalp and eventually causes hair loss. To my knowledge, there are no current studies even exploring scalp DHT’s connection to calcification (even though when we look at broader research, the connection seems obvious).

On top of that, researchers only recently confirmed (in 2016!) that both an increase in androgens and androgen receptors are needed to cause calcification, not just one. This discovery came from cardiovascular researchers and not hair loss researchers. These fields don’t really talk to each other. Neither is very aware of the other’s work. As a result, our third mystery variable remains a mystery.

But even still, we can make a very strong case for what this variable could be.

Uncovering The New Mystery Variable

Here’s what we know: if we inject regular mice with DHT, they develop calcification. But if we inject DHT into mice who can’t produce androgen receptors, no calcification occurs. Why?

Let’s start by looking at the “engineered” mice who can’t express androgen receptors. When they receive DHT, their bodies respond by…

1. Activating proteins associated with calcification inhibition
2. Deactivating proteins associated with calcification induction

In other words, these engineered mice turn on proteins that suppress calcification, and turn off proteins that encourage calcium buildup. The end result: no calcification.

So how do the regular mice – the ones with androgen receptors – respond to a DHT injection? Just the opposite. When these mice receive DHT, their bodies…

1. Turn on proteins that encourage calcium buildup
2. Turn off proteins that usually suppress calcium buildup

The result? Calcified arteries.

This is important. Surrounding our bodies and facial hair, we don’t develop the same calcification or fibrosis that we see in balding regions of the scalp. The same isn’t true for our scalp hair. This suggests one thing:

Our new mystery variable is likely, among other things, an imbalance of calcification regulators.

What Are Calcification Regulators?

Calcification regulators are a set of (mostly) proteins with many names and functions. They regulate whether your tissues accumulate or release calcium. We won’t dive into each of them, but if you want to do more research, here are some examples.

For the calcification inhibitors, there’s…

• fetuin-A
• matrix gla protein
• osteopontin
• osteoprotegerin
• and dozens of others

For the calcification inducers, there’s…

• prostaglandin d2
• transforming growth factor beta 1
• bone morphogenetic protein 2
• bone morphogenetic protein 4
• alkaline phosphatase
• and many more

Not surprisingly, studies have linked each of these “inducers” to hair loss… but no one’s yet identified their relationships to calcification.

The Hair Loss Triple Threat: Increased DHT + Increased Androgen Receptors + Imbalanced Calcification Regulators

Remember, we need three factors for calcification and fibrosis to occur: increased DHT, increased androgen receptors, plus an imbalance of calcification regulators.

This new flowchart checks out against all the available evidence, including the DHT paradox:

A Quick Recap:

1. Androgen receptors (AR) are the places inside our cells where androgens – like DHT – attach themselves. Androgen receptors often turn on or off depending on whether androgens are near. In order for calcification and fibrosis to occur, we need an increase in androgens (DHT) and an increase in androgen receptors.
2. At the same time, there must also be an imbalance of calcification regulators. Calcification regulators are a set of molecules, enzymes, and proteins that control whether our tissues store calcium. There are two categories: calcification inducers (promoters) or calcification inhibitors (suppressors). If our body tissues activate too many inducers and too few inhibitors, calcification will accumulate.
3. Imbalanced calcification regulators explain the DHT paradox – or why DHT encourages hair loss in the scalp but hair growth in the body and face. These regulators stay balanced in hair-bearing body and facial tissues. These don’t calcify. But in the scalp, more inducers than inhibitors activate. The result? Scalp calcification and fibrosis.

We need a combination of all three factors to induce calcification and fibrosis:

1. Increased DHT
2. Increased androgen receptors
3. Imbalanced calcification regulators

Now let’s start tracing this flowchart backwards again.

What could possibly trigger increased DHT, increased androgen receptors, and imbalanced calcification regulators simultaneously?

There are likely two main causes. The first is chronic inflammation. The second is a hormonal imbalance.

Cause #1: Chronic Inflammation

What Is Inflammation?

Inflammation is our bodies’ natural reaction to stressors, like an injury, infection, or toxic chemicals.

For instance, say we stub our toe on a door. Our bodies recognize this injury as a “threat”. Then they activate enzymes, proteins, and hormones to kickstart the healing process. These molecules assess the damage, then determine how much our toe should swell (the pro-inflammatory response) and when to activate repair proteins (the anti-inflammatory response). This is all natural, normal, and healthy.

Chronic inflammation is not healthy. This is when inflammation never resolves – like a virus that won’t go away, or an ulcer that won’t heal. In these cases, inflammation is always present, so our tissues never fully repair. This is the type of inflammation associated with autoimmunity and cancer – and often leads to scarring (read: fibrosis).

Interestingly, increased DHT isn’t just found in balding scalps… It’s also found in inflamed body tissues. There’s even evidence that DHT actually helps regulate inflammation, and that in some tissues, DHT is anti-inflammatory.

This suggests that increased DHT is a part of the inflammatory process. DHT binds to tissues after inflammation occurs. And in our balding regions, if DHT is chronically elevated, our scalps are also probably chronically inflamed.

When we reflect on the causes of calcification and fibrosis, this makes sense. Studies show calcification and fibrosis are both the end-result of chronic inflammation.

Chronic inflammation is the gun. The DHT-AR-calcification regulator imbalance is the trigger.

But there’s one more “gun” that fires calcification and fibrosis… A hormonal imbalance.

Cause #2: Hormonal Imbalance

Hair loss is closely connected to a hormonal imbalance. Specifically, our testosterone:estrogen ratio.

In women, thinning hair has been linked to higher testosterone:estrogen ratios than non-thinning women. In younger balding men, elevated estrogen levels are also common.

But this is just an association… Where does our T:E ratio fall into our flowchart? Evidence shows that this imbalance happens before calcification and fibrosis.

The T:E-Calcification Connection

Our T:E ratio may actually control which calcification regulators our bodies activate.

Remember: if too many calcification inducers and too few calcification inhibitors are active, calcification occurs.

Our body’s T:E ratio is something that helps “regulate” our calcification regulators. If our T:E ratio is imbalanced, we’re at a higher risk of calcification.

This explains why an imbalanced T:E ratio is so strongly associated with heart disease. In men, lower testosterone levels are associated with higher rates of calcification and stroke. Low testosterone men have a near two-fold increase risk in morbidity. They also suffer from higher arterial stiffness (think: fibrosis). Finally, men with higher estrogen levels are also more likely to develop arterial calcification.

In women, low estrogen levels are associated with higher arterial calcification. Women with polycystic ovary syndrome and high testosterone also have higher rates of arterial calcification. The same is true for women receiving testosterone injections after menopause – the time when their estrogen levels plummet.

So let’s add chronic inflammation and an imbalanced T:E ratio to our flowchart:

Now for one final question…

What Triggers Chronic Inflammation And A Testosterone:Estrogen Imbalance?

While there are thousands of factors that contribute to chronic inflammation, an imbalanced T:E ratio, and the conditions that cascade into hair loss, there are four big ones…

Our diet, lifestyle, microbiome, and scalp environment.

For purposes of this article, we’re not going to trace these pillars back any further. The new book covers each pillar in detail – its triggers and what to do about them. For now, here’s the foundation of our hair loss flowchart.

The Master Hair Loss Flowchart

This chart is logic-checked against the scientific literature on DHT, hair loss, calcification, fibrosis, and everything in between. It’s a pretty far step from all the one-line answers doctors tell you, like “DHT causes hair loss” or, “You lose hair when you’re stressed.”

But most importantly, this chart is a tool that allows us to evaluate hair loss treatments. So let’s start using it!

Using The Master Flowchart To Evaluate Hair Loss Drugs

Our flowchart explains not only why a drug like Minoxidil is relatively ineffective at reversing hair loss, but also why Finasteride might be great at stopping hair loss but less effective at regrowing hair. (Note: for a quick overview of Minoxidil and Finasteride, read this).

Minoxidil Versus Our Flowchart

Minoxidil works by providing more blood flow to the follicles. Where is “blood flow” implicated on our flowchart?

Almost right at the bottom (after calcification and fibrosis).

Remember: calcification and fibrosis are chronic, progressive conditions. This means that they don’t go away on their own and they tend to get worse over time.

Increasing blood flow helps our follicles temporarily. But because Minoxidil doesn’t reverse the calcified, fibrotic condition of our scalps, this effect only provides a temporary boost to our hair follicles.

As calcification and fibrosis worsen, Minoxidil’s effectiveness fades.

Finasteride Versus Our Flowchart

Finasteride works by preventing the conversion of free testosterone into DHT. It prevents tissue DHT from accumulating in our scalps. Where does this take place on our flowchart?

Right before calcification and fibrosis.

Since Finasteride reduces DHT in the scalp, it helps stop the cascade of events that trigger calcification, fibrosis, and eventually hair loss…

But because calcification and fibrosis are further downstream to DHT, and because calcification and fibrosis are chronic progressive conditions, then reducing DHT won’t actually reverse these conditions! It’ll only slow or stop their progression. This is why Finasteride is great at arresting hair loss, but not at regrowing much hair.

Try Using The Flowchart!

We can use this flowchart to explain the results and shortcomings of almost every hair loss drug on the market.

If you understand a drug’s mechanism (how it works), you can look at the flowchart and evaluate which part of the hair loss cascade it addresses.

Let’s try it with the drug Spironolactone, a “caffeine” topical, and even a full-on hair transplant.

Spironolactone works by blocking our androgen receptors so that DHT can’t accumulate in our scalps. This might help arrest hair loss, but since it doesn’t address pre-existing calcification or fibrosis, it’s limited in completely reversing the condition.

Caffeine topicals help boost blood flow to our follicles. But decreased blood flow is the result of calcification and fibrosis buildup, and unless we reverse those conditions and their triggers, the benefits of boosted blood flow will be short-lived.

Hair transplants work by transplanting healthy hair follicles from the back of your head to thinning regions. But since thinning regions are ridden with calcification and fibrosis, transplanted hairs may eventually thin too – which is why so many people experience failed hair transplants.

Every treatment’s biggest hurdle is calcification and fibrosis. Without reversing these two chronic progressive conditions, any drug, supplement, topical, or therapy targeting hair loss will only be mildly effective.

Calcification And Fibrosis Are The Two Biggest Hurdles To Hair Recovery

If we want to regrow lost hair, we need to restore the environment of the scalp back to its original state – reversing calcification and fibrosis – and restoring blood flow to dormant follicles so they can turn terminal once again. It’s definitely not an easy path forward, but it’s possible.

Beyond Hair: Why Calcification And Fibrosis Matter

If you’re suffering from hair loss and you think that calcification and fibrosis are only happening on top of your scalp, you’re probably wrong.

Calcification and fibrosis can happen in vessels and soft tissues everywhere in our bodies. And in fact, pattern baldness is closely associated with heart disease. As an article from Harvard states:

“Calcium can accumulate in the arterial plaque that develops after an injury to the vessel wall. The plaque is usually soft to begin with, but eventually tends to harden and become calcified.”

If we eliminate the triggers of calcification and fibrosis, we’re not just targeting hair loss… We’re also helping to halt the progression of calcification in other parts of our bodies. We’re positioning ourselves to become healthier, happier, and longer-living.

It’s Easy To Prevent Calcification. It’s Hard To Reverse It.

It’s much easier to prevent calcification and fibrosis than it is to reverse these conditions.

For instance, the right diet can significantly stop the development of calcification, but diet rarely reverses calcification. This is why, in most cases, dietary changes don’t result in significant hair regrowth. So the next time you see an ad claiming “one simple diet trick” can regrow hair, don’t buy into it.

Final Takeaways

Many people try to make hair loss sound like a “one cause, one solution” problem – but this just isn’t reality.

Calcification and fibrosis are the two biggest hurdles to hair recovery.

Drugs like Finasteride decrease scalp DHT, but they do little to reverse any of the calcification and fibrosis already present in our scalps. As a result, most hair loss drugs only slow or arrest hair loss. They don’t necessarily regrow any hair.

Questions? You can reach me in the comments section any time.

Read time: 10 minutes

Prostaglandin D2 Hits Headlines As A Baldness Breakthrough

In 2012, the dermatology departments of University of Pennsylvania and Johns Hopkins University generated a lot of buzz around a potential “miracle cure” for baldness.

The big discovery? A relationship between prostaglandin D2 (a fatty acid derivative) and male pattern baldness.

The researchers demonstrated, for the first time in humans, that a lipid derivative called prostaglandin D2 was elevated in balding areas – but not in hair-bearing areas – of men with hair loss. More importantly, they also discovered that prostaglandin D2 inhibits hair lengthening. The more prostaglandin D2 present, the shorter a hair grows.

The team suggested that by maybe inhibiting prostaglandin D2 in the scalp, hair loss might be stopped. And that got a lot of hair loss sufferers (and pharmaceutical companies) excited.

Prostaglandin-D2 inhibitors were already in trials as a treatment for asthma. It wouldn’t be hard to develop a topical for men’s scalp using the same technology.

The media went wild, claiming the “cure” for baldness was just around the corner. These researchers began talks with pharmaceutical companies to begin human trials. One article claimed the “cure” for baldness might reach shelves in 2 years. Then came another scientific overview, and even more excitement around the possibility that by inhibiting prostaglandin D2, we might grow back our hair.

Years Later… Is Prostaglandin D2 Still A Hair Loss Miracle?

Today, the buzz around prostaglandin D2 has faded. We haven’t heard much from the human prostaglandin D2 trials. And some of prostaglandin D2’s original hair loss research pioneers have even shifted focus.

So what happened? Does prostaglandin D2 really hold the cure for baldness?

Maybe… Maybe not.

This article uncovers what prostaglandins are, why scientists thought prostaglandin D2 held so much promise for hair recovery, and why prostaglandin D2 might not be the miracle hair loss cure after all.

Important Note: this article was last updated in 2017. Since then, new research has come out clarifying (and contradicting) the role of prostaglandins in androgenic alopecia. As such, this article no longer reflects my exact viewpoints on the subject. We recently published a manuscript about inflammation, prostaglandins and fibrosis – you can read that here.

What Are Prostaglandins?

Prostaglandins are a group of lipids that our bodies generate at sites of injury, like damaged or infected tissues. They are a part of the body’s inflammatory response – meaning that prostaglandins over-express at sites of inflammation.

Prostaglandins have a variety of roles in the “promotion and resolution of inflammation” – like blood flow regulation, blood clot formation, cytokine expression, and even hormone regulation. Their presence changes the way that cells behave – sort of similar to a hormone.

The Bad News About Prostaglandins

In normal amounts, prostaglandins are fine (and even essential). But chronically elevated prostaglandin levels are a bad thing. Prolonged prostaglandin over-expression is associated with more allergies, autoimmune disease, arteriosclerosis, and now even hair loss.

There are many prostaglandin groups – all labeled by their molecular form – but the one that made hair loss headlines was prostaglandin D2 (PGD2).

What Is Prostaglandin D2?

PGD2 is a type of prostaglandin made in our central nervous system and in our skin tissue. On top of hair loss, PGD2 is also the same prostaglandin implicated in asthma. So if you’re also suffering from asthma, you might find the following information relevant.

How Do Our Bodies Make Prostaglandin D2?

Prostaglandin D2 is actually made from another prostaglandin called prostaglandin H2 (I know, the names aren’t that original).

When prostaglandin H2 (PGH2) comes into contact with an enzyme called prostaglandin D2 synthase, it gets converted into prostaglandin D2 (PGD2).

Not All Prostaglandin D2 Hurts Our Hair… Only The Kind That Binds To GPR44

In order for PGD2 to influence cell behavior, it has to bind to a cell’s receptor. There are a few different receptors to which PGD2 can bind, but the PGD2 receptor that’s implicated in hair loss is called GPR44.

When PGD2 binds to the receptor GPR44, hair loss soon follows. This is the one-two combination that hair loss sufferers (and preventers) want to avoid.

Summary So Far: How Prostaglandin D2 Triggers Hair Loss

Prostaglandin D2 is elevated in the bald areas of men with androgenic alopecia. This discovery reinforces previous research showing that in mice, PGD2 increases just before the regression phase of the hair cycle (in other words, prostaglandin D2 increases before hair loss occurs).

Interestingly, researchers also showed that by increasing PGD2 in mice, they can induce hair follicle miniaturization, sebaceous gland hyperplasia, and eventually alopecia. They can use PGD2 to “turn on” pattern hair loss.

So to summarize the the prostaglandin D2-hair loss connection:

1. PGH2 gets converted into PGD2 by the enzyme prostaglandin D2 synthase
2. Then that PGD2 binds to the receptor GPR44
3. For unknown reasons, this triggers hair loss (or more specifically, hair length shortening).

So how can we go about inhibiting PGD2 to protect us against pattern hair loss?

How To Decrease PGD2 (With Drugs)

Two Ways To Stop PGD2: Enzyme Inhibitors & Receptor Antagonists

In order to stop PGD2 from influencing a cell’s function, we need to either…

1. stop PGD2 from ever forming, or…
2. stop PGD2 from binding to a cell

Scientists are developing drugs to do this by…

1. blocking the enzyme that converts PGH2 into PGD2 – prostaglandin D2 synthase. Or…
2. blocking PGD2’s “anti-hair” receptor – GPR44.

Wait… Blocking Enzymes And Receptors Sounds Kind Of Similar To Other Hair Loss Drugs

And it should!

Blocking a substance’s enzyme and receptor is also how hair loss scientists approached reducing another hair loss “culprit”… DHT.

Before PGD2 came along, dihydrotestosterone (DHT) was considered the “cause” of hair loss. The argument was as follows:

In our scalps, testosterone gets converted into DHT by the enzyme 5-alpha reductase. DHT then binds to a cell’s androgen receptor, and for unknown reasons, the hair becomes sensitive to DHT and the follicles eventually shrink, leading to hair loss.

The solution for DHT? Block the 5-alpha reductase enzyme or the androgen receptor to decrease the amount of DHT in our scalps and maybe regrow some hair.

So came the creation of Propecia – a 5-alpha reductase enzyme inhibitor – and Spironolactone – an androgen receptor antagonist (blocker).

Here’s a side-by-side of how PGD2 and DHT form.

Back To PGD2: The Good News For Pharmaceutical Companies

Like DHT inhibitors, a few known prostaglandin D2 inhibitors already exist. Here are a few:

• Setipiprant (a GPR44 receptor antagonist)
• Ramatroban (a GPR44 receptor antagonist)
• Ricinoleic Acid (a prostaglandin D2 synthase enzyme inhibitor). The name sounds scary, but it’s actually just a fatty acid found in castor oil.

So are these PGD2 inhibitors helping us regrow any hair?

Are Prostaglandin D2 (PGD2) Inhibitors Regrowing Any Hair?

PGD2 Clinical Trials… No News Yet

Unfortunately, we haven’t heard word about clinical trial results, nor about the original PGD2 trials from a few years back. This makes me assume that the trials aren’t producing significant signs of hair regrowth.

But there are also non-trial participants – hair loss researchers and forum members who compounded their own PGD2 inhibitors. These experimenters have already begun testing PGD2-inhibiting substances and logging their progress on private hair loss forums. The most common PGD2 inhibitor of choice: Setipripant.

So what are their results?

PGD2 Hair Loss Forum Testers… Not Much (If Any) Regrowth

Some testers are reporting an arrest in hair loss. But unfortunately, none are showing significant signs of regrowth… even after a full year of testing.

But it’s not all bad news.

The Silver Lining: PGD2 Inhibitors + PGE2 Promoters Might Regrow Hair

Some researchers have combined PGD2 receptor blockers with PGE2 promoting substances, and with much better success.

Just check out the regrowth results from Swiss Temples. His “prostaglandin protocol” seems like a bit over-the-top – especially with the safety concerns of some of the substances. But it’s reaping results.

These anecdotes suggest that a PGD2 inhibitor + PGE2 promoter is probably better for hair regrowth, especially versus a PGD2 blocker alone. But based on radio silence from the PGD2 trials and the lacking results from others’ anecdotes – it seems like a PGD2 blocker alone isn’t going to regrow much hair.

Why Aren’t PGD2 Inhibitors Regrowing Much Hair?

While research is still ongoing, it might have to do with that question researchers never answered…

How exactly does prostaglandin D2 cause hair loss?

Maybe the answer is that prostaglandin D2 induces something else… calcification.

Prostaglandin D2 Doesn’t Just Trigger Hair Loss… It Also Triggers Calcification

Calcification is the build-up of calcium deposits in tissues where it doesn’t belong (for example, our soft tissues or our arteries). And studies show that PGD2 is a calcification inducer – meaning that PGD2 triggers calcification.

The bottom line: wherever PGD2 over-expresses, calcification may soon follow.

Calcification Is A Chronic Progressive Condition

The causes of calcification are complex, multifaceted, and not fully understood. But the important takeaway is this:

Calcification is chronic and progressive. If you take away whatever triggers calcification (for example, PGD2), you might stop more calcification from accumulating, but you likely won’t remove the calcification already present.

Scalp Calcification Precedes Hair Loss

The connection between calcification and hair loss was made over 70 years ago when researchers observed in those who were bald, the blood vessels supporting those dormant follicles had become completely calcified.

In fact, calcification precedes hair loss. Calcium buildup in our blood vessels restrict blood flow to our hair follicles, which reduces oxygen and nutrient flow to the follicles. This causes the hair to slowly shrink, until it disappears entirely.

Due To Calcification, PGD2 Inhibitors May Only Stop Hair Loss, But Not Regrow Much Hair

Remember: researchers haven’t yet uncovered exactly how PGD2 causes hair loss. Based on the evidence, my guess is this:

PGD2 induces calcification. That calcification then restricts blood flow to our follicles, until the follicle shrinks and the hair disappears.

If this is true, then it makes perfect sense why a PGD2 inhibitor may only stop future hair loss. If we block PGD2, we prevent future calcification… But we never get rid of the calcification that’s already there.

Why We Should Still Try To Reduce PGD2

It’s still in our best interest to decrease PGD2 expression. Doing so may protect us from hair loss and reduce the symptoms of allergies (and even asthma).

So, is there any way we can go about doing this naturally? Without drugs that haven’t completed the rigor of human trials?

Yes.

How To Reduce PGD2 (Naturally)

Change Your Diet

PGD2 is derived from arachidonic acid, which is an omega 6 fatty acid.

Omega 6 fatty acids are found predominantly in cooking oils (think: canola, olive, safflower, sunflower, and corn), but are also prevalent in many processed foods. They’re considered to activate many pro-inflammatory pathways in the human body.

Going Back To Asthma: Linking Together PGD2, Arachidonic Acid, and Diet

As you ingest higher levels of arachidonic acid, you might also increase the expression of pro-inflammatory messengers in the body – like PGD2. This can lead to a variety of chronic ailments, one of which is asthma.

Conversely, omega 3 fatty acids seem to bolster an anti-inflammatory effect. These fatty acids are found in quality seafood – like wild salmon, scallops, and oysters.

A balance of omega 6 and omega 3 fatty acids help to optimize proper inflammatory responses. Unfortunately, in the case of most first-world diets, people over-consume omega 6 fatty acids and under-consume omega 3 fatty acids.

This was recently evidenced in a large-scale study on children’s diets from 2010. Researchers found that children who ate 3+ burgers a week were at a higher risk for asthma, whereas children who ate more fish and fruits were at a much lower risk.

What’s important to note isn’t that these children were eating burgers… It’s that these children were eating a higher ratio of omega 6 to omega 3 fatty acids (~15:1), and thereby more likely to over-express PGD2 and other inflammatory biomarkers (the indicator being their asthma symptoms). The end-result of prolonged PGD2 expression: breathing problems. The children eating a more balanced ratio omega 6:3 ratio (~4:1) likely expressed less PGD2, and were thereby protected from asthma.

Eat Less Omega 6, Eat More Omega 3

So, if you’re worried you might be over-expressing PGD2, you may want to consume more polyunsaturated omega 3 fatty acids, and consume fewer polyunsaturated omega 6 fatty acids. Doing so might benefit other inflammatory conditions in your body, and even your hair health.

And if you wanted to take this a step further, you can even make efforts increase PGE2.

The One-Two Punch: Decrease PGD2, Increase PGE2 – All Naturally

Remember that the best prostaglandin-related regrowth results so far have been achieved by decreasing PGD2 and increasing PGE2.

We already know that a diet that restricts omega 6 fatty acids may decrease PGD2 expression. But did you also know we can increase PGE2 expression naturally too?

Here to increase PGE2 expression:

Get into the sun as often as possible.

UVB radiation has been shown to upregulate PGE2 expression. All you need to do is start getting into the sun during peak hours of UVB exposure. In doing so, you’ll increase vitamin D and PGE2 expression – which may help tremendously in preventing hair loss (and even regrowing some hair).

Summary Of The Prostaglandin D2-Hair Loss Connection

In 2012, researchers discovered that increases prostaglandin D2 (PGD2) expression reduces hair lengthening. The researchers hypothesized that a PGD2 inhibitor might halt hair loss and even regrow hair.

Unfortunately, we haven’t heard much from the PGD2-inhibitor human trials. On top of that, hair loss forum trials with PGD2 blockers did little more than halt hair loss.

However, some hair loss experimenters are documenting regrowth by both blocking PGD2 and increasing PGE2 expression. The net – if we’re going to try a prostaglandin protocol and we want to maximize our chances for hair regrowth, we need to both decrease PGD2 and increase PGE2.

Fortunately, we can decrease PGD2 and increase PGE2 naturally. Restricting omega 6 fatty acid consumption may decrease PGD2 expression throughout our bodies, and getting UVB radiation (from the sun) can increase PGE2.

And there you have it. I’ll update this article as more news comes out. In the meantime, drop a question in the comments section!

Read time: 10 minutes

The Shampoo-Hair Loss Connection

When I was diagnosed with male pattern hair loss, I immediately went running to Rogaine® and bought a nice shampoo. It’s a natural tendency for people to try and find easy fixes to their problems, and I was no exception.

I kept up this hair loss regimen for years – applying Rogaine twice daily and using a range of shampoos from copper peptides to volumizing thickeners. My hair loss never slowed down. But short of a hair transplant (and subscribing myself to a lifetime of Propecia®), I figured I was doing everything I could to stop my hair from thinning.

I was wrong.

A few years later, I began to rethink my stance on shampooing – particularly after reading ways that shampoos may contribute to hair loss and hair shedding. Yes, much of this research is misrepresented (and overstated) by health websites. At the same time, some of it has merit. And if you’re trying to improve hair health from all angles, you’ll want to at least understand ways in which some hair-washing habits might be contributing to your hair shedding.

A quick personal note: several years ago, I decided to take a break from shampoos and conditioners. I kept this up for four years. During that time, my hair felt and looked a lot healthier. We don’t really need shampoos and conditioners – at least the way we’re “conditioned” to believe. This article explains why.

This article explains the science behind shampooing and its potential connection to hair loss. We’ll uncover the importance of sebum, the dangers of even the most “organic” shampoos, and how to transition away from shampoos without having to worry about dandruff and hair oiliness.

Shampoo Aisle: Paralysis By Analysis

Have you ever walked through a grocery aisle and thought, “Most of these things I don’t even need”?

As consumer packaged goods continue to grow, so do our product choices. This isn’t a good thing. Having more choices doesn’t always make you more informed, better off, healthier, or even happier. In fact, overwhelming someone with too many choices can lead to no choice at all. They even have a name for it… Paralysis by analysis.

There are few better examples of this than the hair care aisle.

What Does The Hair Care Aisle Look Like?

In hair care, it’s common to see product claims attached to every bottle of shampoo or conditioner. Here are a few examples:

• “…extend volume for all-day fullness.” – Garnier
• “…fights fadeouts with zero-weight.” – Pantene
• “…reconstructs at the cellular level.” – Dove
• “…24 hours of defined curls.” – Pantene
• “…lock out frizz for a full 3 days.” – Garnier
• “…fight dandruff.” – Head & Shoulders

Overwhelmed yet? You might need frizz control, or a volume boost, or stronger hair, or all three. What do you buy?

The reality: you don’t really need any of these products. To understand why, you need to understand how hair care products actually work.

How Do Shampoos & Conditioners Work?

Shampoos

Shampoos clean your hair in a couple of ways. First, they strip your hair of any dirt or soil by using a blend of ingredients called surfactants. Surfactants bind with things like dirt, soil, dead skin, and sebum – and when the shampoo is washed away, it takes these things with it.

Shampoos also contain purpose-based ingredients like thickeners, emulsifiers, foaming boosters, scents, and color additives. You can often guess the ingredients in a shampoo by reading the advertising claims on the bottle.

Conditioners

Conditioners are designed to make your hair easier to manage and minimize static. They’ve got ingredients like fatty alcohols and silicones, which help lubricate hair follicles after shampooing cleans them. Conditioners are often used to detangle the hair, make it softer, and make it shinier.

What’s The Problem?

There are three big problems with shampoos and conditioners:

1. Their product claims are often exaggerated and unrealistic. Shampoos and conditioners coat your hair with synthetic compounds that boast the appearance of the claims on their bottles. After a few washes, the effects are gone. That’s why you’ll never see a claim for PERMANENT volume lifts, frizz reduction, dandruff control, or shininess.
2. Their ingredients are carcinogenic and hormone-disrupting. Depending on your frequency of exposure, this can have a compounded negative effect on your health.
3. Shampoos may accelerate the pathway to thinning hair. Shampoo strips your hair of the oils your body naturally produces to protect it. This can worsen the health of your scalp and potentially create the problem of excess sebum production – which, under certain circumstances, may increase inflammation and hair shedding.

But they don’t tell you that on the label.

Shampoos & Conditioners Are Full of Endocrine Disruptors & Carcinogens

The ingredients in most hair care products aren’t always safe. With every wash, you might be exposing yourself to compounds and chemicals known to be carcinogenic and hormone-disrupting. Here are just a few of the common offenders:

1. Parabens

Parabens are manmade preservatives used in cosmetics, pharmaceuticals, personal care products, and (some) processed foods.

Controversy over the safety of parabens began in 2004 when researchers found that parabens were present in 90% of human breast tumors. Not surprisingly, the same parabens in those tumors are also common ingredients in anti-perspiring underarm deodorants used by women. If you haven’t already guessed, parabens penetrate the skin and enter the body when applied topically.

Parabens Disrupt Your Endocrine System

The Environmental Protection Agency’s research suggests consistent long-term paraben exposure can disrupt your endocrine system. Your endocrine system (which is composed of your thyroid, pancreas, andrenals, testes, and ovaries) is absolutely critical to your health. Without a properly functioning endocrine system, hormonal balance is literally impossible.

Endocrine disruptors, like parabens, get stored in your body’s fat tissue and accumulate over time. In the correct concentrations, parabens can bind to estrogen receptors and alter your body’s hormonal secretions, thereby changing the way your body produces and treats hormones.

What does this mean for you? It means that with consistent paraben exposure, you may also have a higher disposition to hormonal imbalances.

Interested in a list of dysfunctions or diseases associated with hormonal imbalances? Here are some highlights:

• Cancer
• Hair Loss
• Cognitive Impairment
• Reduced Immune Functionality
• Anxiety
• Depression
• Osteoporosis

The list could extend a few more pages, but I hope you get the picture. Nobody wants any of those.

Because parabens can negatively sway your body’s testosterone:estrogen ratios, they can also reduce your fertility, depending on the exposure and tissue concentration.

Too Many Parabens Make Men Infertile

The rise in infertility in developed countries has puzzled many scientists, but recent research suggests that increasing levels of male infertility could be the result of higher paraben exposure.

I started minimizing my paraben intake the second I learned that that human sperm was no longer viable after being exposed to 1 mg/mL of parabens. If you’re wondering what our average daily exposure to parabens is, it’s estimated to be 76 mg. Granted this isn’t directly comparable to 1 mg/mL, but I think the context helps show just how little 1 mg/mL really is.

If you’re struggling to conceive, maybe you should consider minimizing your paraben exposure for a few months.

Personal Care Products Account For Most Of Human Paraben Exposure

Since shampoos and conditioners are just one of many sources for paraben contact, you might be wondering why I am cherry picking. Let me be clear: I’m not.

Shampoos and conditioners, alongside other personal care products, account for nearly 70% of our daily paraben intake. Cutting these out will drastically reduce your long-term accumulation of the preservatives, so please consider it.

2. Phthalates

Phthalates are compounds found in plastic water bottles, shampoos, perfumes, shower curtains, body lotions, wood finishers, and hairsprays (to name a few). They’re used to make plastics more flexible and harder to break. Unfortunately, they also harbor unintended and detrimental consequences to our health and hair.

Phthalates are often disguised on labels as “fragrance”, among other terms. Sometimes, phthalates aren’t even listed as an ingredient because they’re only considered a part of a product’s package.

Phthalates Are Ingested Accidentally

Phthalates are often ingested through leaching. Phthalates can leach into foods or liquids heated in plastic containers. You might not think this is a huge deal if you don’t heat things in plastic, but you’d be surprised at how easy it is to ingest high levels of phthalates by accident. For instance, bottled water is full of leached phthalates. Even though the bottles themselves aren’t purposefully heated, they reach temperatures high enough during transportation and distribution to promote leaching into the water. So, even though you never heated that plastic bottle, you’re still likely ingesting phthalates well beyond a recommended limit.

The same is true for shampoos, only this time, you’re rubbing the phthalates directly into your head.

Phthalates Are Also Endocrine-Disrupting

Unsurprisingly, phthalates can also negatively impact your endocrine system by reducing free testosterone levels in the body. Not only that, but phthalates have also been shown to have an estrogenic effect on the body. The mechanisms behind how phthalates reduce testosterone and promote estrogen in the body aren’t fully understood. But the bottom line is, they throw our testosterone:estrogen ratio way out of whack, which means that they can create hormonal imbalances. Once again, hormonal imbalances are linked to a variety of dysfunctions and diseases, two of which are cancer and hair loss. Once again, I’m trying to avoid both of those.

The FDA Knows Phthalates Are Dangerous, But Regulation Is Limited

It’s interesting to note that certain phthalates are banned in children’s’ toys, but not in shampoos. Children also use shampoo, so obviously the FDA didn’t think this legislation through completely. If the FDA were willing to impose regulations on compounds that are dangerous to children, why would those compounds not also be dangerous to adults in higher concentrations?

The truth is, phthalates are dangerous regardless of your age. So avoid them by removing shampoos & conditioners from your hair care regimen.

3. Sulfates

Ever heard of Sodium Laurel/Laureth Sulfate? It’s usually the first ingredient listed in any shampoo or conditioner. It’s a compound derived from coconuts, but the way that it’s processed and extracted creates a multitude of carcinogenic byproducts. Those also end up in the shampoo, though they often aren’t listed. You still rub them into your scalp, and they still accumulate in your body.

Over 16,000 studies have been conducted on sulfates and their byproducts. Research aggregated by the Environmental Working Group suggests the compounds are associated with:

• Developmental/reproductive toxicity
• Organ toxicity
• Endocrine disruption
• Cancers and mutations

Obviously, the relationship between sulfates and these disorders is dose-dependent. Even still, it’s likely in our interests to keep exposures to a healthy minimum – or at least reduce any unnecessary sulfate exposure (through certain shampoos and cosmetic products).

4. Formaldehydes

Do you remember the Johnson & Johnson, “No more tears” campaign for baby shampoos? They reformulated their baby shampoos to be less irritating to babies’ eyes, who have a harder time keeping them closed when getting shampooed. What did they do?

They removed the formaldehyde from their formula.

It’s encouraging to see a large CPG company like J&J take steps toward bettering their products, but it’s disappointing that formaldehydes were used for so long in baby shampoos. Even worse, formaldehydes are carcinogenic. It says so right on the US Department of Labor’s website, and again in a warning they issued to hair salons when reevaluating formaldehydes’ safety in hair care products.

Aside from parabens, phthalates, and formaldehydes, you’ve still got a laundry list of other chemicals you’ll want to avoid (ammonium chloride and methylchloroisothiazolinone, for example).

It’s Likely That Your All-Natural/Organic Shampoo Also Isn’t Very Good For You

You might be thinking, “My shampoo doesn’t have any of these. I am an informed consumer, and I read ingredients lists.” You could be right, but harmful ingredients are just a partial problem with shampoos. Any type of shampoo or conditioner can contribute AND acts as a precursor to pattern hair loss.

While your hair might feel cleaner after washing, shampoos and conditioners actually create an environment in the scalp, which, over a period of time, can significantly contribute to hair loss in both men and women.

Chronic Shampooing May Promote Excess Sebum Production

The scalp produces sebum (natural oil) to keep the hair healthy, shiny, and smooth. At a certain point, the scalp and hair reach homeostasis – enough oil is produced to keep the hair intact, not too dry, and healthy.

Enter shampoos and conditioners. Remember how they clean the scalp? Shampoos strip the hair of dirt, but they also strip the hair of sebum – the natural oils you’re your sebaceous glands excrete to protect the hair. Then, conditioners replace them with synthetic compounds or “natural” oil derivatives.

The scalp, aware of the fact that it has been stripped of sebum, works on overdrive to produce more sebum to keep the hair healthy.

Think about it. Every time you use a shampoo, you wash away the sebum that your body produces to naturally lubricate the hair follicles. It’s an unintended consequence of washing dirt out of your hair, which water can do just fine without stripping the sebum from the hair shafts.

This cycle reinforces itself when we use shampoos over and over again. In turn, our scalps are always churning out more sebum than normal to keep up with the amount lost from shampoos.

The Bad News: Trapped/Excess Sebum Production Might Be Linked To Hair Loss

Research suggests that the build-up of sebum, over time, might indirectly contribute to hair loss. Here’s how.

Sebum is a food source for bacteria that live on our scalps and inside our sebaceous glands. Some of these bacteria are harmless; some are helpful; some are hurtful.

Men with pattern hair loss have higher levels of a harmful bacteria – known as P. Acnes – living on their scalps. Specifically, this bacteria lives inside the sebaceous glands. It eats sebum, and as a byproduct of its digestion, it produces something known as porphyrins. These are toxic substances that react with UV light, which create irritation to trigger an “inflammatory” response from our bodies.

The way our bodies respond? Ironically, by producing more sebum. Unfortunately, this just feeds more P. Acnes, which creates more porphyrins, which creates more inflammation, and the cycle continues.

This cycle is one way that acne can develop. But on the scalp specifically, this cycle may contribute to the inflammation associated with hair shedding. In fact, the presence of pathogenic microorganisms is believed to be one reason why men with hair loss tend to have oilier, shinier scalps.

Unfortunately, when we chronically shampoo (once daily or more), we’re washing away this sebum, which signals to our bodies to produce more of it. This behavior often just exacerbates the problem, as our bodies attempt to send sebum production into overdrive.

This is partly why some people can’t go more than a few days without shampooing. Through chronic shampooing, they’ve conditioned their scalps to overproduce sebum, so after a few days without shampooing, their hair looks wildly oily.

In order to break the cycle, you have to significantly reduce (or abandon) shampoos and conditioners.

Transitioning Away From Shampoos & Conditioners Is Worth It

I did this years ago, and I kept it up for four years. I highly recommend it.

The process takes some adjusting, but I encourage you to stop using all shampoos and conditioners. The transition will take anywhere from 2-6 weeks, but eventually, your sebum production should return to normal and your hair should look much healthier.

For four years, all I did was water-rinse my hair daily. It felt great, and I saved hundreds of dollars on hair products that I really didn’t need.

Note: my experiment ended after I headed a soccer ball that had recently rolled into dog poop. After that, I felt it was time to shampoo. Nowadays, I dilute my shampoo with water and keep my frequency to just a few times week. This works well for me and my hair, and I’d recommend you try the same.

About all else, try to break the habit of chronic shampooing: using shampoo / conditioner products once- or twice-daily. You’re likely doing your hair a disservice… and maybe your health, too.

The Bottom Line: You Probably Don’t Need These Products

Every other species seems to do just fine without shampoos or conditioners. Why are we special? These products are mostly unnecessary. We spend hundreds of dollars on them every year, and yet we shouldn’t. Our bodies evolved with built-in capabilities to maintain a healthy scalp and hair. Why mess with millions of years of trial, error, and evolution?

My hair looked great during my years of no-shampoo. Once your scalp adjusts, I don’t think you’ll regret the switch.