The Scalp Tension Theory Of Hair Loss: A Scientific Breakdown

Rob Misc. Research 28 Comments

Can Scalp Tension Cause Hair Loss? It’s Possible.

Is there a connection between scalp tension and pattern hair loss (androgenic alopecia)? Sixty years ago, researchers thought no. Today, many are changing their tune.

The scalp tightness theory recently regained popularity in hair loss forums, but it isn’t new. Over 100 years ago, Bernarr Macfadden noted an association between scalp tightness and androgenic alopecia (AGA) in his book Hair Culture. And in 1950, the scalp tension theory of hair loss even advanced into the academia. For the next decade, androgenic alopecia researchers supported its plausibility.

Then in 1959, everything changed. Most of the scalp tightness theory’s advocates turned from supportive to dismissive… and almost overnight.

What happened? Why did researchers change their minds?

Well, a series of hair transplantation studies were published that contradicted the scalp tightness theory of androgenic alopecia. This led researchers to assess the evidence, reevaluate their opinions, and abandon the scalp tightness theory altogether. For the next forty years, the idea that scalp tension could cause hair loss remained “unrealistic.”

That is, until recently.

In the last five years, new studies have emerged that are forcing researchers to reevaluate the scalp tension-androgenic alopecia hypothesis yet again. These studies not only help build a biological rationale for the scalp tightness hypothesis, but they also present evidence opposing the counterarguments of theory.

So what are these studies? And what’s making researchers waver yet again? This article series explains it all.

This is a three-part series on the scalp tightness theory of hair loss. In this article, we’ll uncover the science behind scalp tension and its potential relationship to pattern hair loss.

In the next article, we’ll dive into the debate over this theory. After all, a few studies from the 50’s and 70’s seemingly contradicted the theory entirely. But now – over forty years later, new evidence is challenging these counterarguments… and bringing the debate back to life again.

In the last article, we’ll try to settle this debate and uncover where scalp tension might come from. Does scalp tightness cause androgenic alopecia? Is scalp tension merely associative with hair loss? And if does cause pattern hair loss… what can we do about it? As always, when it comes to hair loss research, the answers aren’t so cut-and-dry.

Scalp Tension Theory: The Basics

We’ll soon get into the details of the scalp tension-androgenic alopecia hypothesis. For now, here are the basic principles.

Skin tension tends to restrict blood flow to tissues – much like a bent finger tightens our knuckle and turns it white. Interestingly, research suggests that balding men and women tend to have chronically tighter scalps than those without hair loss.

Across the body, excessive tissue tension can evoke an inflammatory response which, if left unresolved, leads to scar tissue formation. We’ve seen this in stressed periodontal ligaments, the eyelids of patients with Graves’ disease, enlarged prostates, and in the hand tissues of people with Dupuytren’s contracture. The bottom line: more tissue tension, more inflammation, more scar tissue.

As scar tissue settles in, it simultaneously restricts blood, oxygen, and nutrients to tissues. Fascinatingly, the same phenomena and observations – tissue tension, inflammation, reduced blood flow, lower oxygen, and increased scar tissue – are also seen in balding scalps. In fact, we see the onset of these observations in the same pattern and progression as hair loss.

Interestingly, studies on scarring-related diseases – like scleroderma – reveal that once enough scarring settles, hair cannot grow. Putting it all together, this suggests that scalp tension might be involved in the inflammatory cascade which leads to pattern hair loss.

Tension evokes inflammation, inflammation evokes scar tissue, scar tissue restricts oxygen and nutrients to the hair follicles, and this slowly miniaturizes the hair follicles until eventually… we’re left with pattern baldness. Thus, in its most basic form, the scalp tightness-androgenic alopecia theory looks something like this:

Scalp tissue tension >> inflammation >> scar tissue >> pattern hair loss

Does the scalp tension theory differ from our current understanding of androgenic alopecia?

Yes and no. The scalp tightness-hair loss theory fits well in the literature, and of what we already know about androgenic alopecia (or AGA). In fact, it might even enhance our understanding of AGA.

To get a full picture of why, we need to understand…

  1. The current model of AGA pathology (what researchers currently believe is the cause of AGA).
  2. Questions this AGA model cannot answer
  3. How the scalp tension theory answers these questions while still making sense of previous findings in AGA research.

Let’s take these one-by-one.

What Causes AGA? Our Current Understandings

AGA is the world’s most common hair loss disorder – affecting 50% of women and 80% of men throughout a lifetime. And it’s unique because it only affects a certain region: the top part of our scalps.

In men, the hair loss often begins at the temples and vertex. In women, it begins as more globalized (diffuse) thinning. In both genders, the condition is chronic and progressive – meaning that with time and without treatment, it will continue to worsen.

If you’ve ever looked into the causes of AGA, you’ve probably come across the term dihydrotestosterone, or DHT. DHT is a hormone that’s made from testosterone. In fact, most dermatologists will tell you that an interaction of our genetics and DHT is what causes pattern hair loss. Hence the medical name, androgenic alopecia. Andro = androgens; genic = genes; alopecia = hair loss.

So is there any truth to this claim? Yes. There’s an overwhelming amount of evidence that DHT is causally linked to pattern hair loss.

Firstly, studies show that DHT is higher in the scalps of men with thinning hair. Secondly, if a man is castrated, his testosterone (and DHT) levels plummet permanently. Men castrated before puberty (i.e., before their DHT levels spike) don’t go bald later in life. And thirdly, men with a genetic deficiency in an enzyme that converts testosterone into DHT in scalp tissues never develop pattern hair loss.

DHT Shrinks Hair Follicles

These are pretty indicting findings. Just look at the endpoints: men who never produce DHT never develop pattern hair loss. Men with higher amounts of DHT in their scalps have AGA. Based on these findings, DHT must play some causal role in AGA.

But beyond that, things start to get complicated…

DHT is causally linked to AGA. But eliminating DHT doesn’t lead to a complete hair recovery

Finasteride is an FDA-approved drug that men use to help fight AGA. It works by reducing DHT levels. In fact, when taken as prescribed, finasteride can reduce scalp DHT levels by over 60%.

But just how effective is it at treating AGA?

Well, clinical studies suggest finasteride improves hair loss outcomes for 80-90% of users. That means it helps slow, stop, or partially reverse hair loss for 80-90% of the people taking it. But just how much hair can we expect to recover?

Over a two-year period, those same studies suggest that finasteride, on average, leads to just a 10% increase in hair count – with hair count plateauing thereafter.

This suggests that finasteride is mostly limited to stopping hair loss progression, rather than reversing the condition entirely. Similar observations were made in castrates. Castration (and thereby near-full DHT reduction) only seems to stop pattern baldness. It doesn’t fully reverse it.

And therein lies the first big “question” of the DHT-hair loss hypothesis.

Question: If DHT causes pattern hair loss, how come eliminating DHT only stops AGA? How come it doesn’t lead to a full hair recovery?

This actually isn’t impossible to answer.

Many researchers have hypothesized that this may be due to DHT’s relationship with scar tissue. In scalp tissues, the arrival of DHT seems to also remodel our scalps – causing increased disorganized collagen crosshatchings. In other words, scalp DHT causes fibrosis (or scarring).

In fact, balding scalp regions have four times the amount of excess collagen deposition (scar tissue) than non-balding regions. And as we’ve learned in scleroderma studies, where there’s scar tissue, hair cannot grow.

DHT >> scar tissue >> hair loss

So maybe the reason why eliminating DHT doesn’t fully reverse hair loss… is simply because stopping DHT only stops the progression of scar tissue. It doesn’t necessarily reverse the scar tissue already present.

This makes sense. In fact, this is the explanation many AGA researchers use to describe why our recovery from AGA is “limited”. But interestingly, this explanation brings up another question that the DHT-hair loss theory has a much harder time answering.

Question: If DHT causes scarring and hair loss in the scalp… why does DHT encourage hair growth in other parts of the body?

Why does DHT encourage hair loss in the scalp… but hair growth in the chest and face?

You may have noticed that a lot of bald men also have incredibly hairy bodies. Well, this is because DHT can have two totally opposite effects on hair. It all depends on its location in the body.

For instance, studies show that while DHT in our scalps appears to encourage hair loss, DHT in body tissues (i.e., facial and chest skin) appears to encourage hair growth.

How can that be? How can DHT encourage hair growth in secondary body and facial hair… while simultaneously encouraging hair loss in our scalps?

Unfortunately, this is something the current DHT-androgenic alopecia pathology model cannot explain. So its supporters chalk it up to genetics – explaining it must be due to gene variants that are associated with more androgen receptors and their co-activators.

There’s some truth to this, but the reality is that nearly every single cell in our body carries the exact same genes. What differentiates a cornea cell from a skin cell is the combined influence of gene programming + a cell’s environment.

This means that “genetics” is sort of a blanket explanation for things we don’t understand. Not only is it the go-to answer for questions that exceed our knowledge base… it also completely undermines the influence of environment – which is often half (or more) of the equation.

In fact, there are several more questions that the DHT-AGA pathology model answers with the idea of “genetics” – but in reality, isn’t as supported by the literature as most tend to believe. Here they are:

Question #1: what causes DHT to increase in balding scalp tissues in the first place?

Question #2: why does DHT encourage hair loss in the scalp… but secondary hair growth in the body and face?

Question #3: why is there a pattern to AGA? Why does it begin at the temples and vertex for most men and generalized thinning for most women?

Question #4: why does AGA only affect the top part of our scalps – in areas that overlie the dense fibrous membrane known as the galea aponeurotica?

So, is it possible to answer these unanswered questions of AGA pathology, and in doing so, create a better model to explain the causes of pattern hair loss… all while not undermining any research demonstrating that DHT is causally linked to AGA?

Potentially. This is where the scalp tension theory of hair loss comes into play.

Scalp Tightness-Pattern Hair Loss Theory: A Deep-Dive

In 2017, I reintroduced the scalp tightness theory in a scholarly paper – particularly in light of new studies that reinforce its role in AGA. The rest of this article will explain the basics of that paper.

The best place to start is to attempt to provide answer those unanswered questions – and beyond “genetics”. Our first question: why does DHT increase in balding scalps?

Question #1: Why does DHT increase in balding scalps?

To get an idea of what might cause DHT to increase in balding scalp tissues, we need to have a bigger picture of what’s going on balding scalp tissues. That means it’s worth cataloguing most of the observations researchers have seen in balding scalps.

We’ve already discussed a few of these – like DHT and scar tissue. But there are many other things happening, too. And if we know what they are, maybe we can begin to parcel out a cause-and-effect relationship between balding scalps and increased DHT.

Here are the big ones from the paper.

Biological. Balding scalps have higher levels of androgen activity – specifically, DHT. And interestingly, balding scalps also express higher amounts of inflammation. We see this in the form of specific signaling proteins and reactive oxygen species (more on this later). These are things that commonly arrive in sites of “stress” – i.e., where the body senses an injury or an infection.

Physiological. Balding scalps have four-fold more disorganized collagen fibers (i.e., scar tissue) than non-balding scalps. And interestingly, the patterning and progression of this scar tissue appears to match the patterning and progression of AGA. In other words, where we see an increase in disorganized collagen cross-hatchings, we also see hair loss. Moreover, we also see that balding scalps have lower blood flow and lower oxygen levels than non-balding tissues – and that in all likelihood, the reduced blood flow occurs outside of our natural hair cycling.

Structural. Several dermatologists and AGA researchers have noted, anecdotally, that balding scalps appear to just “feel” tighter than non-balding scalps. This was also discussed by Dr. Brian Freund – a former university lecturer and hair loss researcher. He mentioned that his male and female patients with AGA almost always had incredibly tight scalps. There’s some evidence that this tension may come from involuntary contractions from our scalp’s perimeter muscles – which would pull the top of the scalp tightly – much like bending a finger pulls the knuckles tight.

Now that we have a better understanding of what’s going on in a balding scalp, we can revisit that initial question:

What causes DHT to increase in balding scalp tissues?

After all, maybe the answer is in one of these observations…

Clue #1: DHT is anti-inflammatory

Beyond its role in sexual maturation, studies also show that DHT can over-express in tissues as a response to inflammation – and that specifically, DHT is anti-inflammatory.

This is incredibly telling, especially in regard to androgenic alopecia research. After all, balding scalps show both increased inflammation and increased DHT. Maybe the inflammation observed in balding scalp tissues is what causes DHT to increase.

However, this opens a new question. If inflammation is what causes DHT to increase in balding scalps… what causes inflammation in the first place?

Reflecting back on our catalogue, there’s at least one possible culprit: chronic tissue tension.

Clue #2: tissue tension can “activate” inflammation and DHT

The relationship between tension, inflammation, and androgen activity isn’t very shocking. In fact, it’s been observed in several other regions. For instance…

  1. Inflamed periodontal tissues can signal to increase androgen activity.
  2. Men with a tendon-contracting condition known as Dupuytren’s contracture also express more inflammation and male hormones in the affected tissues.
  3. Graves’ disease sufferers often have chronic eyelid retraction due to the involuntary contraction of the Mueller muscle). In biopsies, this muscle shows higher markers of inflammation and often androgen activity.
  4. Prostate tissues, when exposed to cyclical stretching, induce inflammation and DHT-induced transforming growth factor beta-1 (more on that later).

All of this suggests that in balding scalps, chronic tension may induce the arrival of inflammation and DHT. To put it simply:

Chronic tension >> inflammation >> DHT

Now that we’ve have a potential reason for the “arrival” of DHT, we can ask a harder question:

Why is DHT linked to hair loss in the scalp… but hair growth in other body regions?

Fascinatingly, tension might also help explain this DHT paradox. Here’s how.

Chronic tension and androgens can induce scar tissue

Research shows that DHT behaves differently depending on its location. Specifically, DHT can increase hair loss in the scalp but also increase hair growth in the best and face. This suggests, at a minimum, that a tissue’s location has some sort of influence on the effects of DHT.

So, can tissue tension help us answer this DHT paradox?


When DHT in chest and facial tissues, it induces more hair growth. But when DHT is expressed in the scalp – i.e., in tissues under chronic tension – DHT induces the arrival of a signaling protein called transforming growth factor beta 1 (or TGFβ-1).

This is interesting, because DHT doesn’t always appear to induce this signaling protein in tissues that aren’t under added contraction.

However, we do see DHT-induced TGFβ-1 in periodontal tissues, Dupreyene’s contracture, and in benign prostate hyperplasia. And fascinatingly, we also see DHT induce TGFB-1 in balding scalp dermal papilla cells (i.e., the cell clusters that influence the size of our hair follicle).

This signaling protein – TGFβ-1 – is universally condemned across biology as a biomarker for aging, and more specifically, as a prerequisite for the onset of fibrosis (scar tissue).

Studies have shown that wherever TGFβ-1 over-expresses, fibrosis soon follows. And as a reminder, balding scalps have four-fold more disorganized collagen crosshatchings (i.e., fibrosis) than non-balding scalps.

In fact, this scar tissue seems to develop alongside the pattern and progression of AGA. For men, it begins at the temples and vertex… and spreads to the rest of the scalp in accordance with hair follicle miniaturization.

The DHT-hair loss hypothesis suggests that fibrosis might be what limits our ability to regrow hair. But if fibrosis actually causes hair follicle miniaturization, then this would explain why DHT grows hair in the chest and face… but leads to hair loss in the scalp.

So, is there evidence that fibrosis or excess collagen deposition leads to baldness?


Excess collagen (or scar tissue) can prevent hair growth

In the medical literature, one defining characteristic of scar tissue (i.e., fibrosis) is the absence of hair. In fibrosis-related disorders (like scleroderma), researchers have consistently observed that as fibrosis sets in, hair loss soon follows – even in the scalp.

And in this article, I lay out a few step-processes behind how fibrosis might contribute to hair follicle miniaturization. The gist is that excess collagen appears to onset outside of normal hair cycling and it seems to progress throughout hair follicle miniaturization – implying that its presence may possibly explain the production of smaller hairs in AGA.

This suggests that in AGA, fibrosis may cause hair loss, and through a few mechanisms: firstly, through the constriction of space for a hair follicle to grow. And secondly, through tissue degradation. Specifically, the restriction of blood, oxygen, and nutrients to the hair follicles.

DHT >> TGFβ-1 >> fibrosis >> reduced blood and oxygen >> hair loss

Taking a step back, DHT’s opposing “behavior” in the scalp versus the body might be explainable through the evidence that…

  1. In the presence of chronic tension, DHT induces signaling proteins which lead to scar tissue (and thereby hair follicle miniaturization)
  2. In the absence of chronic tension, DHT doesn’t induce these signaling proteins… so it simply encourages hair growth.

This is a subtle difference, but with potentially huge implications in the world of AGA. And we can now add these findings to our revised AGA model.

Chronic tension >> inflammatory response >> DHT >> TGFβ-1 >> fibrosis >> restricted blood flow >> hair follicle miniaturization >> pattern hair loss

However, there’s still one outstanding question… can tension also explain the pattern and progression of AGA? And if so, can it explain the differences in thinning patterns for both men and women?

The evidence points to yes.

Scalp tension may also explain the pattern and progression of AGA

In men with AGA, hair loss often starts at the temples and vertex. And fascinatingly, we also see this same patterning with scalp tension.

There are certain modeling softwares that allow us to estimate the tensile force of any surface – so long as we know the surface area and the direction and magnitude of forces applied to that surface.

In 2015, researchers decided to use a modeling software to map the tensile projections of the tops of male scalps. The forces applied to that surface? The contractions of the scalp perimeter muscles – the same chronic contractions noted by Dr. Brian Freund and other AGA researchers.

The findings? A near-perfect correlation between scalp tension peaks, the patterning of AGA, and the progression of male pattern hair loss. For a graphic reference…


Since scar tissue also onsets in the pattern and progression of male AGA – this perfectly aligns with the idea that scalp tension might be the beginning of the hair loss cascade.

But what about women?

Unlike most men, most women don’t start thinning at the temples or vertex. Rather, they tend to lose hair in a diffuse pattern.

And what about hair loss that occurs in advanced stages of AGA – like hair loss we see at the nape of the neck, or behind the ears? Could tension also explain this?

Preliminary research points to yes.

In fact, other investigators have used the same modeling software to “play” with these tension projections. What they’ve found is that by making small tweaks head shape, size, and contraction force, it’s possible to create tensile patterns that match the pattern of hair loss we see in women.

In fact, it’s also possible to do the same for more advanced stages of AGA – like hair loss above the ears and at the nape of the neck. One researcher even shared his findings for free – which you can access here.

Where might this scalp tension come from?

This is going to be saved for another article. The short answer is that there are likely three major sources of scalp tension, and each creates a feedback loop with the others:

  1. The chronic involuntary contraction of muscles surrounding the perimeter of our scalps. Specifically, the muscles connected to the galea aponeurotica.
  2. Skull bone growth and skull suture settlement during and after puberty.
  3. Fascia remodeling surrounding the galea and its connected tissue networks.

Tying it all together – genetics, scalp tension, and AGA

This is a lot of information, and as such, it might help to see a visualization of everything above. As such, here’s the flowchart that I presented in my paper:

I know we didn’t cover every aspect on this flowchart. Doing so would’ve made this post twice as long. But I hope you can see the logic progression, and how everything ties together:

Scalp tension >> inflammation >> DHT >> TGFβ-1 >> fibrosis >> restricted blood flow >> hair follicle miniaturization >> pattern hair loss

So if scalp tension is a contributor to AGA… does relieving scalp tension improve AGA outcomes?


Dr. Brian Freund demonstrated that in AGA sufferers, botox injections to relieve tension in chronically contracted scalp muscles increased hair counts by 18%. And this year, a new study confirmed Dr. Freund’s original findings. Finally, tension offloading devices also appear to improve hair growth in AGA subjects over 3-12 months periods. So at a minimum, it seems like targeting scalp tension improves hair growth in men and women with AGA.

Does the scalp tightness-hair loss hypothesis fit into all of the literature on AGA?

At face-value, the AGA theory of scalp tension satisfies the questions left unanswered in the current DHT-hair loss pathology model.

  1. Why does DHT increase in balding scalp tissues? It increased as part of an inflammatory response, and this inflammation is mediated by skin tension.
  2. Why is DHT associated with scalp hair loss and body hair growth? If expressed while under tension, DHT induces the expression of transforming growth factor beta 1, which leads to scarring and thereby hair loss. This tension is present in the scalp, but not in body tissues.
  3. Why is there a specific pattern and progression to AGA? This patterning matches the tensile patterning and progression of scalp tissues – with the highest tension points as the first to suffer from hair loss.

But does the scalp tightness-AGA theory make sense of all aspects of AGA research?

Not necessarily.

The reality is that I just presented the entire scalp tension argument to you in a bubble. I didn’t yet  introduce a layer of complexity that, at first glance, could dismantle the theory entirely.

There is a complication to the scalp tightness hypothesis: a compelling counterargument. And it’s a big one. It’s the early findings from hair transplantation studies.

The scalp tension counterargument: hair transplantations

Remember in 1950 – when the scalp tension hypothesis made its way into academia? And in 1959 – how the scalp tightness theory was swiftly abandoned?

This is because that year (and the years following), researchers published several studies on hair transplants which completely changed the trajectory of hair loss research.

These studies sought to confirm if going bald had anything to do with the environment of our scalp tissues. Specifically, things like scalp tension.

To test this question, researchers decided to transplant skin grafts containing healthy hair into balding regions… and take skin grafts containing balding hair and transplant them into other parts of the body.

The findings? If we transplant hair follicles to or from a balding region…

  1. Non-thinning hairs moved to balding scalps keep growing normally.
  2. Thinning hairs moved to non-thinning regions keep thinning… at the same rate as thinning scalp hairs.

What did this suggest? That our scalp environment has nothing to do with balding.

Otherwise, why would thinning hairs transplanted out of a tense scalp environment keep thinning – even when placed in non-thinning regions? And why would healthy hairs transplanted into a tense environment keep growing – even as the hairs around them continue to thin?

This led researchers to abandon the scalp tension hypothesis, and instead conclude that baldness must be due to genetic programming within the hair follicle itself.

This idea of genetic determinism has been the prevailing theory for the last sixty years… until recently. Now new studies are making us question whether we drew the right conclusions about hair follicle miniaturization all those years ago.

And what are those studies? That’s for the next article.

Scalp Tension Summary

Research shows that balding men and women tend to have tighter scalp tissues than their non-balding counterparts. And interestingly, this scalp tension tends to align with the pattern and progression of AGA.

In men, tension is the highest where hair loss first begins (i.e., the vertex and temples), with skin tension dissipating alongside the “spread” of pattern hair loss. In women, equal tension can be modeled throughout the scalp skin – similar to a diffuse thinning pattern.

When our bodies sense a stressor (i.e., a cut, an impact, or an infection), they evoke an inflammatory response. Interestingly, this is also true for tissues under chronic tension. DHT has been shown to be anti-inflammatory, and when a tissue is under chronic tension, DHT tends to over-express. We’ve seen this in several disease states related to involuntary contractions. Resultantly, chronic scalp tension might not only explain the inflammatory biomarkers we see in balding scalps, but also the arrival of DHT (something the DHT-gene theory of AGA does not satisfactorily answer).

In cases where DHT is activated through tension, we also see DHT induce a signaling protein that causes scarring; specifically, TGFβ-1. This creates excess collagen deposition and scarring (or fibrosis), which then restricts blood, nutrient, and oxygen supplies to the affected tissues.

Interestingly, we see all of the above in balding tissues: increased DHT, increased TGFβ-1, increased fibrosis, lower blood flow, and lower oxygen levels… and in the exact same patterning as AGA.

Studies on scarring-related diseases demonstrate that where scar tissue accumulates, hair does not grow. And evidence suggests that fibrosis in our scalps may precede hair thinning. As fibrosis accumulates, this would cause hair follicle miniaturization through space restrictions alongside tissue degradation (i.e., reduced blood supply). The end-result: hair thinning in the pattern of AGA.

The scalp tension-AGA hypothesis, in my opinion, is the only hypothesis that satisfactorily makes sense of these unanswered questions in AGA research: 1) why does DHT increase in balding scalps, 2) why does DHT encourage hair loss and hair growth depending on its tissue location, and 3) why is there a “pattern” to pattern hair loss?

Unfortunately, hair transplantation studies from fifty years ago led researchers to conclude that our scalp environment – and specifically, scalp tension – have nothing to do with the onset of pattern hair loss. This led to the abandonment of the theory…

Until recently. In the next article, we’ll uncover why.

Note: Regardless of the evidence for or against scalp tension, there are potentially dozens of other factors kickstarting the inflammatory cascade that leads to hair loss. Therefore, scalp tension – if it truly does cause hair thinning – is just a contributor (and not a root cause). Future articles will explain why.

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.

Powered by ConvertKit

Comments 28

  1. Pingback: Do Hair Transplants Debunk The Scalp Tension-Hair Loss Hypothesis?

  2. Many clues have led me to believe that hairloss is more than genes. Ur articles make me believe that. My friend once commented that my scalp is white. Ur article explains this being due to tightness and it doesn’t receive nutrients. Also diet being a huge factor. Im on the edge of buying your book. There are days when i believe that i can completely reverse hairloss with natural ways but days when i think its not possible. If i could get ur email Rob id ask you a few questions and then decide should i buy ur book

    1. Post

      Hey Ahmed,

      Thanks for reaching out! If you opt into the email course (mentioned at the end of the article), my email is in there. As a heads up — I’m very behind on emails and am doing my best to catch up. But my current priorities are focused on packaging all of our findings from the last two years into another book update. So my availability for email follow-up, at least right now, is very spotty! I apologize.


  3. I posted this on another article, but I’m not sure if it went through.

    Rob, i’d like to say that I really enjoy that you take care to address inconsistencies and critiques of your believes on hair loss. I think we only refine our ideas and make them stronger when we face the other side of our beliefs. I feel like you want to get to the truth, no matter where it might be, not just be right. I look forward to the next article in this series detailing how transplant studies seem to counter the scalp tension theory.

    On another topic what do you think about obstructive sleep apnea and its role in hair loss? Could it be a potential cause or factor of AGA in your opinion? I’ve read, though unreliable sources, that untreated sleep apnea can damage the capillaries in your scalp. I used to have a full head of hair 5-6 years ago but then I gained over 100 pounds (for various reasons, it’s a long story) and I’ve been receding and thinning pretty rapidly while the rest of my family has their full heads of hair (even my parents and my living grandparents). I’m starting to treat my sleep apnea and while I have not recovered hair growth at all, I’ve noticed my hair looks better and the existing hair feels/looks a bit thicker after a few months of treatment. Any thoughts on sleep apnea and hair loss?

    1. That’s interesting K, I’ve had insomnia for years. Probably around the time my hair loss started. But not sure if that would be a trigger for me.

    2. Post

      Hey Kamran,

      Thanks for the kind words. I saw your comment in the other article, and will respond to both here.

      Sleep apnea certainly hurts overall health by decreasing overall oxygen levels. Oxygen is required for the conversion of free testosterone into estradiol (which is much more “hair-friendly” in scalp tissues). In lower-oxygenated environments, our tissues actually favor the conversion of free testosterone into DHT — since this conversion doesn’t require oxygen. So with this logic, low circulating oxygen levels (from sleep apnea and other sources) might decrease scalp tissue oxygen and thereby encourage the conversion of scalp tissue DHT — which wouldn’t help our hair.

      But there are a lot of extrapolations with the above, and at the end of the day, it’s hard to determine causality between the two — at least with the literature we have currently.

      Congrats on the improvements so far! Please keep us posted with your progress. I’d love to see before-after photos as your hair continues to change from treating sleep apnea — it’d make for a great case study to show researchers (anecdotes are usually how many researchers decide to start studying / exploring these kinds of relationships).


  4. Hi Rob, can you do an article and the role of masturbation and hair loss. I heard because of excessive masturbation prolactin rises which causes excessive inflammation in our bodies which causes many outcomes such as psoriasis, hair loss etc.

    1. Post

      Hey Anton,

      This is part of the FAQ section in the book, but I’m happy to cover it in a future article. The gist is that I don’t see a connection between the two, but if there is a connection, it’s likely at the extremes.

      Prolactin-related hair loss is a very specific type of hair loss and not necessarily related to androgenic alopecia. So if masturbation does raise prolactin levels in scalp tissues (I’ve yet to see evidence of this beyond theoretical serum prolactin increases), it would likely cause shedding rather than AGA.


  5. Hi Rob. i have only one question to you. causes hair loss from each region in women. All regions. Side Crown Hill Nape. Why is it different from men? What are the androgen-free factors in hair loss. ?

    1. Post

      Hey Nurr,

      This is often indicative of telogen effluvium, alopecia areata, or hair loss related to an underlying condition (like hypothyroidism). The good news is that if you can target the underlying factors here, you can often reverse those types of hair loss (since they’re generally non-scarring).


  6. Dear Sir !


    I am a customer who have newly start the massage therapy after purchasing your program. (Book + Demonstration Video @ 49$ ).

    As it seems a hard work for hairloss sufferers to work hard for about 10 months to regrow hairs, but it worth it.

    Why i am commenting you is that i like research in this field like you, and want to ask you a question and want you to do more research on this topic. Have you ever wondered or have thought in a different way that which people in this universe have healthiest hairs ? i have think about it and seem that people who they smoke Crack have the healthiest hairs on the planet. They even don’t wash their hairs in a 2 months period and their heads are full of dust and soil because of sleeping near the roads during the nights, and you know what ? they eat a very unhealthy diet and breath the very dusty air ! i live in Kabul, Afghanistan(Top in pollution)

    Still they have the healthiest full head of hairs on the planet. What is the missing key Rob ? you are a researcher but haven’t looked at this yet i think. Please let me know if you have any understandings about this topic, or if you don’t have any information related this, please investigate and find the real reason behind this. You maybe the first one who could find a perfect solution from the drug Crack for hair loss sufferers or for bald heads.

    Thanks and let me know about your opinion.

    1. Post

      Hey Jordan — thanks for reaching out.

      I think there’s a confounding factor: crackheads look twice their age. Resultantly, they may give off the impression that they’ve maintained full hair density throughout older age (40-60), when in actuality, they’re closer to 20-30.

      I used to think the same about the homeless in San Francisco until I spoke with a friend who worked in city planning. He interacted with a lot of homeless for his job, and often told me they’re much younger than they appear. In my opinion, this is probably the biggest factor. Although I could be wrong!


  7. Hello,

    I have onset of baldness, I lose my hair at the temples. However, it’s not only in this part that I lose my hair. I also lose them in the neck. Can you explain to me what this is about? I’m very worried.

    I would like to send you some pictures by email. Can you give me your email address.


    1. Post

      Hey Brooks — without more information, it’s really hard to say what’s going on. Technically, muscular contraction creates tension in two directions which can explaining thinning behind the ears and the nape of the neck. However, you might also have an underlying condition causing the thinning (hypothyroidism, etc.). While I no longer have the time to review photos / engage in in-depth email support, I’m happy to discuss your situation over a Skype consult:


  8. But all hormones and blood tests are normal. Shedding continues for 7 years. Is it possible to be AGA? I have miniaturization in my hair. Short, long, thick, thin all my hair is dumped. But there is shedding from every region. What do you think? Your ideas are very important to me.

    1. Post

      Hey Nurr — unfortunately, serum tests rarely correlate well with hormonal conversions in periphery tissues (like the scalp). The same is true with nutrients. Given the length of time that you’ve been shedding, I tend to suspect that if AGA isn’t involved, there has to be some other underlying condition that your lab tests haven’t yet revealed.

      For what it’s worth, most doctor-ordered lab tests tell us nothing. I see this time and time again in consultations — especially with diffuse thinners. Someone will come in with “perfect” serum lab tests according to their doctor. Then I’ll ask them to follow up with a stool analysis, breath test, and more comprehensive blood work. The next round of testing usually reveals a heavy metal overload, a SIBO infection, etc. And it’s only by targeting those that we see any resolution to their shedding.


  9. Hi Rob,

    I love the site and find the information provided in this article and throughout your book/site to be very compelling.

    If this theory is correct, it seems that chronic contraction of the scalp perimeter muscles plays a primary role in the process of hair loss. I’ve read about people who have had success using botox to help reverse hair loss, which fits neatly into this theory of hair loss. My question: Do you know of any natural alternatives that can similarly relax the scalp perimeter muscles and prevent chronic tension?


    1. Post

      Hey Matt,

      Thanks for the kind words. And it’s a great question. Pressure-based massages and acupuncture can also relax these muscles. It takes a while to retrain them / become aware of when they’re “tight” — but if you know where these muscles underly, you can begin to knead the perimeter of your scalp and really loosen them up. For a lot of readers, it’s made the difference between regrowth / no regrowth.


  10. Hey Rob,

    Great job again, I’m routinely following your work here. Also purchased the book just to support your efforts in a small way. I’m also planning to share my results within a couple of months to contribute to your data set.

    I have been doing the massages for around 10 months. They gave great results in relaxing the scalp and getting rid of the thickening. My actual question is, aside from that detumescence paper, how do we now the sufficient amount of time to spend on these massages? I have seen in Youtube people using wooden brushes for around 4 minutes, twice daily, and obtaining very similar scalp conditions. I actually like the massages and I normally watch documentaries while doing them to double up the benefits. But just wonder if there is a scientific reason to say that 20 or so minutes is more beneficial then 4 minutes with these brushes. In fact, I tried the brush myself for these last couple of days, and it really is easier to generate the pressure with these thinner than finger bristles and also gives you a great blood rush for around 10 minutes just like the way we want in normal massages.

    I just wanted to clarify this because I honestly believe that you could on the verge of a big understanding of the mechanism and propose a reliable, easy to grasp way of reversing AGA. If we can make the mechanostimulation more convenient, we can also increase the number of people jumping to the ship and immensely enlarge the data set. I think your hypothesis on the causation of AGA is already good enough with the supporting evidence but we need more justification on the optimization of the mechanical approach to reverse it. Thanks in advance if you can find the time to reply.

    1. I’ve been doing a combined routine with Rob’s method (the warmup section) with a bit of scalp shaking and the wood bristle brush the last few months and getting good results. Total about 5 minutes in the evening and 2-3 minutes in morning. I think Rob’s method is a bit better at loosening the scalp although I haven’t tried just doing the brush either, don’t want to break a working routine!

      As for the brush, holding it down just firm enough so it doesn’t slide across the scalp and making circular motions seems to really get in there, simultaneously pinching and stretching the scalp, and the wooden bristles really get the blood flow going – just do the same on the inside of your forearm and you’ll see the skin goes red instantly. I think the method makes sense and it feels great.

      1. Hey Jim,

        Thanks for the reply. My main concern about the brush was that, when I was brushing regularly, too many follicles would fall. But as you said, when you just fix it at a point and move the scalp circularly with it, it simulates that pinching and pressing action more efficiently without stripping the hair. I also agree that Rob’s massage is more effective in relaxing the skin. So, I actually liked the idea of combining the massage for the relaxation of the skin and the brush for the acute inflammation for a much shorter and as effective routine. I’m guessing, as you mentioned again, around 3-4 minutes of finger tip massage followed by a 3 minute brush rotation, two times a day would be a really nice routine.

  11. Hi Rob
    Thank you for the very well researched articles. There’s been a lot hype lately around using derma rollers to encourage blood flow to the scalp. What are your thoughts on using them? I apologize if you have already covered this topic before.

  12. Hi Rob!

    I have a question about minoxidil and vasoconstriction. If this is the main effect of rogain etc, and theoretically massaging is also attending to blood flow issues, what are your thoughts on topical (and perhaps oral) CBD in contributing to blood flow, as well as seratonin regulation and nutrient absorbition? Using a coconut oil cbd infused topical for about a week or two now has shown incredible improvements on face and scalp skin and I use during scalp massages, hoping it contributes something.

    Your thoughts are appreciated

  13. Hi. Thanks for the article. I’m wondering, do you know anything about histamine in relation to MPB? I believe there may be a link between hayfever, sensitivity to histamine/over-production of histamine and MPB. Probably tied in to the inflammatory/tension factors associated with MPB.


  14. Hey Rob,

    We know that an inflammation in causes hairloss! Maybe according to your theory it might be due to scalp tension. But the question arises that if i do a 20 minute massage once or twice daily, wouldn’t it create an inflammation in hairfollicle causing more hair miniaturisation and hairfall? Also, wouldn’t it trigger more DHT production as an anti inflammatory response to the inflamation? Even if the blood circulation improves but the inflammation stays. isnt it?

  15. I’ve been doing the messages for almost a year now. After experiencing a few false starts due to my technique, I’ve actually seen some progress of late (loosening of scalp, less itching). Unfortunately, I have begun to experience pain in upper-chest muscles (My subclavius muscles to be exact – Look up on Google images for reference) I was wondering whether anybody else has experienced this?

  16. Hi Rob,

    Excellent article as usual, thanks for sharing.

    I really am struggling with this scalp tension theory and was hoping you could answer something for me.

    Why is it that the areas on my scalp that are the tightest, also have the most hair? For instance at the back of my head where the neck muscles meet the skull, the skin is super tight but the hair there is super thick. This would be considered the “donor area” for HT. My mid-scalp is also tight but good density.

    Areas on the side of my head (also donor) are loose, but so are the temples and vertex where I have been thinning for years. Does this contradict the scalp tension theory?

  17. Okay, so i just found this video and in life you can see many more examples

    Of guys who have all their hair, even this guy has a very good hairline and yet hes is incredibly unhealthy. So there goes any kind of real connection with having your hormone regulators being imbalanced, inflammation, lack of blood flow etc that you are trying to piece together and prove.
    And as you can see, his dad also has a full head of hair so im afraid its purely genetic. Hair loss is not our fault, i do not want to keep feeling depressed on the idea that i played a part in my own balding process of being unhealthy in some way and that i could have prevented it because there is too much evidence to show thats its purely genetic amd most likely your hair follicles are pre-determined at birth to die at a certain age, nothing to do with tight scalp, or calcification etc because otherwise how can you explain these theories on this guy in the video?

    A hair system is the only way to go or a transplant if you can have the coverage.

Leave a Reply

Your email address will not be published. Required fields are marked *