Read time: 20 minutes
Men Who Transition To Women Regrow Hair… But How?
When Bruce Jenner transitioned to Caitlyn Jenner, many people noticed a change in Caitlyn’s hair quality. During and after the transition, her hair grew thicker and longer. Her temple recession even filled in — giving the appearance of what looked like a juvenile hair line.
It’s easy to assume Caitlyn’s hair regrowth was due to a cover-up spray, hair transplant, or even a wig. After all, Caitlyn Jenner is a celebrity — with the means to afford all three.
But if we dive deeper into the research, that assumption might be wrong. Many male-to-female transexuals and transgenders achieve significant hair regrowth during and after their transition. Some even experience near-complete hair recoveries — from slick bald to a thick, full head of hair.
Here’s just one (of many) examples of male-to-female major hair recovery.
This regrowth occurred during her gender transition — after beginning something known as hormone replacement therapy. This involves taking drugs to increase female hormones (like estrogen) and decrease male hormones (like testosterone and DHT) circulating in the body.
That’s real hair regrowth — and without a cover-up spray, a hair transplant, or a wig. And this degree of hair regrowth is incredible — for two reasons.
First, it dispels the myth that once hair is lost, it’s gone forever. Secondly, it baffles hair loss researchers. Why? Because according to them, hair loss is caused by a male hormone called dihydrotesterone (DHT) — and while eliminating DHT should slow, stop, or partially reverse hair loss… it shouldn’t result in full hair recoveries.
But trans male-to-females taking hormone replacement therapy are both eliminating DHT and recovering massive amounts of hair. The question is… how? Nearly all hair loss researchers say these results aren’t explainable by the literature — or our current understandings of the causes (and treatments) of pattern hair loss…
…except that’s not true. These results are explainable by the literature. We just need to do some digging.
The short-answer: hair regrowth from male-to-female hormone replacement therapy has less to do with eliminating DHT… and more to do with hormone replacement therapy’s one-two punch: eliminating DHT + increasing estrogen. The end-result: the skull bone structural changes and the atrophy of scalp muscle, both of which lead to the relief of chronic scalp tension — the very tension that is the precursor to scalp inflammation that kicks off the DHT-hair loss cascade. When this chronic scalp tension disappears, hair begins to regrow.
This article uncovers the science. We’ll explain exactly why male-to-female hormone replacement therapy leads to major (or sometimes complete) hair regrowth, why DHT-reducing drugs don’t, and what this means for future hair loss treatments.
Along the way, we’ll uncover…
- Misunderstandings. What researchers get wrong about the causes of hair loss
- Questions. If DHT causes hair loss, then why don’t DHT-inhibiting drugs regrow all lost hair?
- Evidence. The real drivers of hair loss (structural tension + an inflammatory response)
- Answers. How male-to-female hormone replacement therapy addresses both hair loss drivers
Note: this article gets technical. If you have questions, you can reach me any time in the comments.
What Is Male-To-Female Hormone Replacement Therapy?
Male-to-female (MTF) hormone replacement therapy is when we manipulate our amount of hormones circulating so that estrogens increase and androgens (like DHT and testosterone) decrease.
HRT’s rationale is as-follows: in humans, hormones play a major role in sexual dimorphism — or the physical differences between men and women. Around puberty, boys’ testicles begin producing more testosterone, and girls’ ovaries begin producing more estrogen.
These difference in hormone production then affects tissue function. Testosterone and its byproducts (like DHT) fuel bone growth and muscular development — along with the onset of chest and facial hair. Conversely, estrogen fuels the onset of menstruation, and the development of a “female figure” — like retention of more subcutaneous fat and even breast development.
These hormones subtly (and not-so-subtly) affect our tissues, until they eventually culminate into the different physiques we attribute to men and women.
As such, male to female hormone replacement therapy attempts to replicate a female’s hormonal profile inside a biological male — in hopes that the person undergoing the therapy will appear more female
And it works. Studies show that when we manipulate a male’s hormonal profile to produce more estrogen and less testosterone — that male begins to take on the attributes we commonly associate with women (facial structure changes, breast development, etc.).
To achieve this, male-to-female hormone replacement therapy (HRT) users sometimes…
- Inject (or supplement with) estrogens — typically in the form of estradiol.
- Take anti-androgenic drugs — like spironolactone — to reduce testosterone and DHT
- Undergo gender reassignment surgery to remove the penis and testes. This reduces testosterone production by 95% (and DHT production by roughly the same)
Interestingly, one side effect of male-to-female hormone replacement therapy is massive hair regrowth… which is why this therapy fascinates (and baffles) most hair loss scientists. And it’s why I wrote this article.
Hair Loss And The Hormone Replacement Therapy Paradox
We’re attempting to answer one of the most challenging paradoxes in hair loss research:
If the male hormone DHT causes hair loss, but DHT-inhibiting drugs like Propecia only stop or partially reverse hair loss… then how come hormone replacement therapy for male-to-female trans patients (reducing DHT + increasing estrogen) can lead to near-full hair recoveries?
I know that’s a mouthful, so let’s slow down the hormone replacement therapy (HRT) paradox more:
- Research shows the male hormone dihydrotestosterone (DHT) causes hair loss…
- …but research also shows that stopping DHT production doesn’t regrow all lost hair. It typically just stops hair loss, and sometimes leads to partial hair recoveries.
- However, male-to-female HRT patients (who take drugs to decrease DHT and increase estrogen) have achieved full hair recoveries.
- The question is… why? If DHT causes hair loss, but reducing DHT typically only stops hair loss… then how come reducing DHT + increasing estrogen can lead to major hair regrowth?
This is a complex and caveated question — with a complex and caveated answer. And in order to explain why MTF hormone replacement therapy regrows hair, we actually need to answer two questions:
- First — if DHT causes hair loss, why doesn’t stopping DHT production regrow all lost hair?
- Secondly — how can stopping DHT production + increasing estrogen lead to full regrowth?
In the next few sections, we’ll tackle that first question. We’ll reveal the evidence behind the “DHT causes hair loss” claim. Then we’ll explain why that claim is wrong. Finally we’ll uncover the two likely drivers of hair loss — calcification and fibrosis — where DHT fits in, and how calcification and fibrosis explain why stopping DHT halts hair loss, but doesn’t necessarily reverse it.
Once we cover those bases, we can explain the science behind the HRT-hair regrowth paradox.
Hormones & Hair Loss: The DHT-Causes-Hair Loss Theory
What causes pattern hair loss — the hair thinning that men experience after puberty, and women experience after menopause? Most doctors (and researchers) believe that pattern hair loss is caused by a hormone called dihydrotestosterone — or DHT.
I first heard about DHT after being diagnosed with pattern hair loss in 2007. My doctor’s explanation: for reasons not entirely understood, DHT begins to accumulate in our scalps. Our hair follicles then become sensitive to this DHT, and as a result, begin miniaturizing. Over a series of hair cycles, this leads to thinner hair until eventually that hair is too thin to see — and we’re diagnosed with pattern baldness.
When I asked my doctor why men bald more often than women, he said that this was simply due to to the fact that men have more androgens (like DHT and testosterone) than women. When I asked him why men bald in a unique pattern, he replied that no one knows (remember that — it’ll be relevant later).
Evidence That DHT Causes Hair Loss
There are three findings that (sort of) cement the DHT-hair loss hypothesis:
- DHT is higher in the tissues surrounding balding hair follicles.
- When a man is castrated, his testosterone (and DHT) levels permanently decrease. Men castrated before puberty (before their DHT levels increase) don’t suffer from pattern hair loss later in life.
- Some men lack the enzyme needed to convert testosterone into DHT in the scalp. Men with this genetic disorder don’t develop pattern hair loss — but they do look more feminine (since DHT is a masculinizing hormone).
At first glance, this hypothesis seems airtight. Look at the extremes: if we never produce any DHT, we never develop pattern hair loss. Conversely, hair loss develops as scalp tissue DHT increases.
These findings were why pharmaceutical companies began targeting DHT to treat hair loss. So came the creation of finasteride (Propecia) — a DHT-reducing drug.
Propecia can reduce scalp DHT levels by up to 70% (depending on the dosage). It’s an incredibly effective DHT inhibitor — and as a result, an incredibly focused hair loss treatment.
So, let’s logic-check the science.
If DHT is truly the sole cause of hair loss, then by reducing DHT with Propecia, we should be able to regrow the hair we lost. Right?
Wrong. While the literature suggests this should be possible, clinical trials on DHT-reducing drugs show a different result.
Evidence Against The “DHT Causes Hair Loss” Hypothesis
Despite DHT’s implication in the development of pattern hair loss, DHT-reducing drugs like Finasteride typically only slow, stop, or partially reverse hair thinning. They rarely — if ever — lead to full hair recoveries (even at the highest daily dosages).
In fact, we can push this even further. What happens if we’re suffering from pattern hair loss, and rather than attenuate DHT with a drug, we just eliminate it entirely? Will we regrow our hair?
We can find our answer by reading studies of men who were experiencing pattern hair loss and then got castrated. Castration reduces circulating testosterone levels by 95%, and since testosterone is a precursor to DHT, castration also plummets DHT production to nearly nothing.
So did these male pattern hair loss sufferers — who then got castrated — regrow all of their hair? No. They merely stopped their hair loss — with minimal (if any) significant hair regrowth.
This suggests that while DHT is absolutely implicated in the progression of pattern hair loss, eliminating DHT isn’t an effective treatment for hair loss reversal. And this also reveals two unanswered questions in the DHT-causes-hair loss theory:
- Why does DHT in our scalps start increasing in the first place?
- If DHT allegedly “shrinks” our follicles, then why doesn’t removing DHT regrow all lost hair?
Hair loss researchers don’t have the answers, but other fields that also study DHT do. And once we take into account all research on DHT spanning hair loss, endocrinology, and cardiology, we realize that…
DHT probably doesn’t directly cause hair loss. But DHT contributes to the development of two chronic conditions: calcification and fibrosis. And when these two conditions develop in the scalp, they restrict blood flow to the affected tissues — starving them of blood, oxygen, and nutrient supply — thereby leading to the degradation of what those tissues support — our hair.
I promise this is all relevant to male-to-female hormone replacement therapy. Stay with me!
The DHT-Calcification-Fibrosis Connection
Hair loss and heart disease are closely associated. In fact, pattern hair loss is a predictive determinant in a person’s risk for heart disease. Could these two conditions share the same mechanism of action?
The answer: yes. Heart disease is commonly characterized as the narrowing of our arteries — and thereby the reduction of blood flow to and from our heart. According to the research, two major drivers of this arterial narrowing is the accumulation of fibrosis and calcification inside the arteries themselves — leading to the restriction of blood flow.
Calcification is essentially calcium deposits in unwanted places — like our soft tissues (blood vessels and capillary networks). This impedes blood flow. Fibrosis is essentially scarring — or the accumulation of collagen fibers in a tissue. If you’ve ever gotten a cut that left a scar, that scarring is fibrosis (the imperfect accumulation of collagen).
Interestingly, calcification and fibrosis are also implicated in pattern hair loss.
The DHT-Hair Loss-Heart Disease Connection
Cardiologists have long suspect that androgens — like DHT — contribute to heart disease. Why? Because studies done in vivo (in life) show that testosterone and DHT injections can increase arterial calcified lesions by 200-400%. And this increase in DHT can also lead to increased fibrosis in heart tissues.
In other words — DHT appears to be a prerequisite for the arrival of both arterial fibrosis and arterial calcification. And here’s where it gets interesting: fibrosis and calcification are chronic, progressive conditions. They very rarely improve or reverse with medications. They tend to get worse over a series of years.
And even more interestingly, calcification and fibrosis don’t reverse when we stop DHT production… even though DHT helps contribute to the development of both conditions.
DHT Causes Fibrosis And Calcification; Fibrosis And Calcification Cause Pattern Hair Loss
As it turns out, fibrosis and calcification are documented all over balding scalp tissues and inside the blood vessels supporting thinning hair follicles. And studies suggests these conditions cause hair loss — not DHT.
For purposes of this article, we’re not going to go into the overwhelming evidence supporting the DHT-fibrosis-calcification-hair loss theory. If you’re curious about the research, read this article.
Rather, I’m going to summarize the takeaways from the above-mentioned article so that we can get back to answering the question: why do so many male-to-female hormone replacement therapy patients regrow all of their hair?
The net: DHT doesn’t directly cause hair loss. Chronically elevated scalp DHT (alongside other variables) causes scalp fibrosis and scalp calcification, and those two conditions cause hair loss by restricting blood, nutrient, and oxygen supply to our hair follicles.
Fibrosis and calcification develop slowly over a number of years. They don’t go away by reducing DHT. And now that we’ve covered this, we’ve just answered the first-half of the male-to-female hormone replacement therapy paradox:
Question: if DHT causes hair loss, then why do DHT-inhibiting drugs like finasteride (Propecia) only stop our hair loss or partially regrow lost hair, but rarely (if ever) lead to full hair recoveries?
Answer: because DHT doesn’t directly cause hair loss. But DHT does cause fibrosis and calcification — two chronic, progressive conditions that reduce blood, oxygen, and nutrient flow to the tissues they affect. Calcification and fibrosis appear to be the main drivers of pattern hair loss. If we inhibit DHT… we stop the progression of calcification and fibrosis, but we don’t really remove much of the calcification and fibrosis already present. This is why DHT-reducing drugs stop hair loss, but don’t lead to full hair regrowth.
Now that we’ve covered that, we can begin to answer our real question:
If stopping DHT production only stops hair loss… then how come male-to-female hormone replacement therapy (stopping DHT production + increasing estrogen) can fully regrow hair?
The Evidence: Trans HRT (Stopping DHT + Increasing Estrogen) Can Lead To Significant Hair Regrowth
Remember those studies on men who suffered from male pattern baldness and were then castrated? They stopped losing their hair, but didn’t regrow much of their lost hair. But that’s not the entire story…
…Because those same studies showed that when castrated men were injected with estrogen, they began regrowing significant amounts of hair. Or in other words, men suffering from pattern baldness who 1) stopped DHT production, then 2) increased estrogen — made major hair recoveries.
Those studies were done decades ago, and now their results are also occurring in male-to-female hormone replacement therapy patients who are basically doing the same thing (increasing estrogen, stopping DHT production).
In fact, here’s another example of the efficacy of increasing estrogen + reducing DHT production. While the following hair loss sufferers’ intention wasn’t to transition from male to female, they did end up taking the same drugs many use to gender transition, and as a result, saw similar hair regrowth:
So what’s the explanation behind these results? Why does stopping DHT production + increasing estrogen lead to major hair regrowth, while simply stopping DHT production only stops hair loss?
The short-answer: stopping DHT production + increasing estrogen remodels skull bone structure, and in doing so, indirectly relieves chronic tension in the scalp skin — the same chronic tension that precipitates scalp inflammation and thereby the DHT-hair loss cascade.
Or in other words, trans male-to-female hormone replacement therapy fixes the two major underlying drivers of pattern hair loss, and in doing so, regrows an incredible amount of hair.
In this second-half of the article, we’re going to explain exactly how this happens. And to answer that, we’ll need to…
- Explain the connection between chronic tension, inflammation, DHT, and hair loss
- Reveal the causes of chronic scalp tension: 1) muscular overdevelopment, 2) skull bone growth
- Explain how DHT-reducing drugs can remodel bone structure — but not to the degree required for full tension relief (and thereby full hair regrowth)
- Uncover how male-to-female hormone replacement therapy 1) atrophies the muscles around the scalp and 2) changes skull bone structure, and in doing so, alleviates chronic scalp skin tension
- Explain why this is the perfect hair regrowth recipe — and why full hair regrowth for male-to-female HRT patients isn’t paradoxical — it actually makes complete sense.
Let’s take these one-by-one.
Chronic Scalp Tension, Inflammation, DHT, And Hair Loss
Note: there’s an overwhelming amount of research showing that chronic scalp skin tension is the major driver in pattern hair loss development. To keep this post shorter than a novel, I’m only going to highlight a few relevant studies. If you’re interested in a major overview of the scalp tension-hair loss connection, please read this article.
A 2015 hair loss study showed that balding scalp regions corresponded with hair loss sufferer’s highest scalp skin tension points — the vertex and the temples.
The authors also showed that chronic skin tension can upregulate androgen activity, in addition to signaling proteins that encourage the development of fibrosis. In fact, this same study demonstrated that scalp skin with the highest chronic tension was not only balding, it was also fusing with fibrotic material with the underlying layers of the scalp (the galea).
Why is this important? Well, let’s take this into the context of the hormone DHT — the alleged “cause” of pattern hair loss.
What does this all suggest? That DHT increases in our scalps, simply because it’s a part of our bodies’ inflammatory response.
Here’s the order of events:
In our scalps, chronic scalp skin tension turns on pro-inflammatory signaling proteins. These signaling proteins then send inflammation to our scalp tissues. Our bodies respond to that inflammation by sending DHT — a hormone with anti-inflammatory properties — to the inflamed tissues. But since this inflammation is from chronic tension — and not an acute injury — DHT cannot resolve it. As a result, DHT chronically stays elevated in the scalp skin. And unfortunately, chronically elevated DHT (along with other factors) ends up causing fibrosis and calcification, which then cause hair miniaturization.
One more time, step-by-step:
- Chronic scalp skin tension turns on pro-inflammatory signaling proteins
- Pro-inflammatory signaling proteins send inflammation to our scalps
- Our bodies respond to the inflammation by sending DHT to our scalps
- Rather than resolve the inflammation, DHT instead forms calcification and fibrosis
- Calcification and fibrosis restrict blood, nutrient, and oxygen supply — which leads to hair loss
No wonder why DHT-inhibiting drugs don’t regrow much hair. They only address the response to inflammation… and not the actual cause of the inflammation: chronic scalp skin tension.
And before we can explore what causes chronic scalp skin tension, we need to do a logic-check — just like we did with the DHT-hair loss hypothesis.
If Scalp Skin Tension Causes The Inflammation Which Causes Hair Loss… Then If We Eliminate Scalp Skin Tension, Can We Reverse Hair Loss?
While the research is still in its infancy, all signs suggest yes. If we eliminate scalp skin tension, we not only stop hair loss — but we can likely reverse it — meaning full or near-full hair recoveries.
In fact, there are studies testing rather crude ways of relieving chronic scalp tension — and its effects on hair regrowth.
One study hypothesized that chronic scalp tension was in part due to the overdevelopment of muscles surrounding the perimeter of the scalp. The study revealed that by injecting these muscles with botox — and essentially “forcing” them to stay relaxed — hair count increased ~20% over 48-weeks:
Another study tested a tension-relieving device on balding men. The device pushed the scalp skin upward in order to relieve the chronic tension along the temples and vertex. The data showed that the longer the device was worn, the more regrowth occurred for the individual testing it.
So if relieving scalp tension leads to regrowth — with time-dependent results based on the duration of tension relief — then this begs the question…
What Causes Scalp Tension In the First Place?
There are several hypotheses, but in my opinion there are likely two major contributors:
- The overdevelopment of muscles surrounding the scalp (continuously pulling tight the scalp skin). This has been at least partially confirmed by the above Botox study.
- Skull bone growth (which creates constant tension across the top part of our scalps). This is evident even at birth — when babies show male pattern baldness until their cranial sutures shift and their hair slowly fills in over a series of 3-5 years. In addition, Paul Taylor also wrote a theory about skull bone growth causing pattern hair loss — which you can read here, or my critique here.
In any case, the evidence is clear that skull structure informs chronic scalp tension, and that chronic scalp tension informs the pattern and degree of hair loss.
And this means that we can boil down the causes of hair loss to a simple two-part equation:
Structural Tension + Inflammatory Response = Pattern Baldness
The structural tension: either 1) overdeveloped muscles surrounding the scalp, or 2) undesired scalp skull bone growth. Either of these scenarios creates chronic tension — the same tension we observe in scalp skin. And that tension creates an inflammatory cascade on the scalp.
The inflammatory response: this is largely where epigenetics and genetic predisposition come into play. Not all bodies respond to inflammation with DHT. In fact, our genes largely determine how much DHT arrives at an inflammatory site, and how long it stays.
It takes chronic scalp skin tension + an inflammatory response to trigger pattern hair loss. And as a result, any effective treatment needs to tackle both 1) structurally-caused scalp tension (scalp bone structure + scalp muscle overdevelopment), and 2) the inflammatory response (the DHT cascade).
Enter male-to-female hormone replacement therapy. And ignoring all side effects, this is probably the most effective therapy for reversing male pattern baldness.
Why? Because MTF hormone replacement therapy likely 1) changes our skull bone structure and atrophies scalp muscles, and 2) eliminates DHT production so that we stop responding to inflammation with DHT.
Male-To-Female Hormone Replacement Therapy May Remodel Facial And Skull Bone Structure
- Testosterone is needed to encourage bone formation
- Estrogen is needed to suppress bone resorption and turnover
- Both testosterone, estrogen, and the ratios of testosterone:estrogen inform bone structure
So, what happens in adults when we start playing around with hormone levels? We start seeing bone structural changes.
This should be no surprise for some Propecia users — who’ve reported facial structural changes as a side effect of the DHT-inhibiting drug. Propecia can inhibit DHT to near-castration levels, and depending on how long someone takes it, facial structural changes are likely unavoidable.
With that said, those changes from Propecia appear minimal — and likely don’t move the needle enough to relieve chronic scalp tension. Rather, since Propecia is exclusively targeted toward inhibiting DHT — it only really helps with the second-half of our hair loss equation: attenuating “the DHT response”.
Propecia Doesn’t Change Bone Structure That Much… But MTF Hormone Replacement Therapy Might
Changes to bone size, density, and structure are observed in postmenopausal women taking long-term hormone replacement therapy to increase estrogen. And improvements to bone fragility are also observed in low-testosterone men taking hormone replacement therapy to increase testosterone.
This suggests it’s likely for male-to-female transgenders and transexuals — especially 1+ years into their transition — to also undergo a degree of bone structural, density, or mineralization changes. And these changes are likely to present in the face and skull (and potentially affect pattern hair loss).
First, just look at the profile differences of male versus female skull bones:
Then let’s refer back to our MTF hormone replacement therapy example. See how this person’s facial bone structure changes throughout their 12-month transition. Their jawline softens, their face narrows, and their frontal bossoming (bone protrusion at the forehead) even decreases.
Without question, this is the result of hormone replacement therapy: a near-arrest of testosterone and DHT production + an increase in estrogen. It’s likely that these subtle changes to skull structure have some sort of impact on the structural tension of the scalp — and that during these bone changes — much of that tension is relieved.
And this therapy does something else too…
Male-To-Female Hormone Replacement Therapy Atrophies The Muscles Surrounding The Scalp (Which Relaxes It)
Muscle growth is fueled by both testosterone and DHT. Unfortunately for Propecia users — while Propecia can reduce DHT (and thereby hair loss), it doesn’t do much to atrophy the muscles surrounding the scalp that are contributing to scalp tension.
Why? Because Propecia only reduces DHT — not testosterone (in fact, Propecia increases testosterone and estrogen by roughly equal percentages). As a result, Propecia really only targets one of the major determiners of muscle growth (DHT) — rather both major determiners (DHT and testosterone).
Conversely, male-to-female trans hormone replacement therapy targets to reduce both testosterone and DHT. How? By either 1) taking drugs that reduce total testosterone production, or 2) castration — whereby testosterone production decreases by 95% and DHT by roughly the same.
This has serious effects on muscular atrophy. Again — just look at those above photos of MTF HRT hair regrowth success. We see 1) an atrophy of muscles in the face, and 2) a change to skull bone density and/or structure. Both of these likely relieve chronic scalp tension, and thereby lead to major improvements in hair loss.
Skull Bone Changes + Muscular Atrophy May Reverse Chronic Scalp Tension And Thereby Encourage Full Hair Regrowth
And this is why it makes sense to see major hair recoveries from MTF hormone replacement therapy. It’s not paradoxical. In fact, it’s expected — and fits perfectly with the body of evidence on pattern hair loss etiology.
It all has to do with the MTF HRT addressing the underlying causes of hair loss: chronic structural tension + a chronic inflammatory response. While Propecia might address the second-half of that equation, it does little (if anything) relieve scalp tension — and therefore the drug is merely a bandaid to prevent future hair loss.
What Does This Mean For Future Hair Loss Treatments?
It means that hair loss drugs, supplements, and topicals that target to…
- Reduce signaling proteins associated with inflammation (like transforming growth factor beta)
- Reduce prostaglandins (like prostaglandin D2)
- Reduce DHT (like Propecia)
…will only help slow, stop, or partially reverse hair loss. They’ll never lead to full hair recoveries. This has been demonstrated — time and time again — with every single male pattern hair loss treatment study. The results are never that impressive.
This also partially explains why drug companies have yet to develop drugs to reverse calcification and fibrosis — particularly for hair loss. Why? Because when it comes to reversing scalp calcification and fibrosis — these conditions are due to chronic tension. If a future drug will reverse scalp calcification and fibrosis, it’ll do it by targeting chronic scalp tension — not a single signaling protein that contributes to either .
We Can Reverse Fibrosis (And Maybe Hair Loss) By Relieving Chronic Tension
Here’s the kicker: dozens of studies now demonstrate that by relieving tension in inflamed or fibrotic-ridden tissues — the body begins to metabolize that fibrotic material, and instead replace it with healthy, unscarred tissue.
What does this mean? The best way to reverse hair loss likely isn’t with drugs, topicals, or surgeries. It’s by relieving chronic scalp tension. If we do that, we shut off the inflammatory cascade — including reducing DHT and all those pro-inflammatory signaling proteins naturally — and give our hair a fighting chance to regrow.
That doesn’t mean that all men need to undergo male-to-female hormone replacement therapy to see hair regrowth. It just means that we should find therapies that target the scalp’s chronic structural tension and the subsequent inflammatory response.
Summary: Trans Hormone Replacement Therapy, Hair Regrowth, And Why Propecia Doesn’t Get The Same Results
Pattern hair loss is essentially a two-part equation: 1) structural changes to the scalp that evoke inflammation (overdevelopment of the muscles lining the scalp + skull bone growth), and 2) our bodies reaction to that inflammation (ie: whether we send DHT to the inflamed tissues).
For hair loss to occur, we need both chronic structural tension + a DHT response. This creates the conditions necessary for calcification and fibrosis to develop. Over time, these two conditions eventually starve the hair follicles of oxygen, blood, and nutrients — causing them to miniaturize.
Male-to-female hormone replacement therapy resolves both sides of this equation. When a male transitions to a female with hormone replacement therapy, they shut down DHT production and increase estrogen. This likely does two key things: 1) it eliminates chronic scalp skin tension by a) slightly changing skull bone density and structure, and b) atrophying the muscles surrounding the scalp which pull the skin tight. And 2) MTF hormone replacement therapy reduces the likelihood of DHT being sent as a response to any inflammation — since the liver cannot produce as much DHT anymore because the testes (which produce testosterone, the precursor to DHT) are either suppressed or gone.
As a result, trans MTF hormone replacement therapy often gets better hair regrowth results than any drug, supplement, topical, or hair transplant.
Unfortunately, Finasteride resolves only one half of one part of the hair loss equation — the amount of DHT arriving at inflamed balding scalp tissues.
Finasteride may slightly influence bone and muscular structure — but not enough to resolve chronic structural scalp tension. As a result, Finasteride is more of a bandaid to hair loss. It slows, stops, or sometimes partially reverses hair loss… but because it doesn’t relieve chronic tension, it’s not a solution to reversing any of the scalp calcification or fibrosis already present.
The biggest takeaway from these male-to-female hormone replacement therapy case studies: we need to start targeting both sides of the hair loss equation (structural tension + inflammatory response), and not just one.
Stop Googling "How To Regrow Hair" Until 3AM
Instead, just sign up for my 10-day course on natural hair recovery.
You'll get access to my before-after photos, the science behind the DHT paradox, hair loss mistakes to avoid, reader-submitted photos, and more.