Hair Loss (AGA) And Low Blood Flow: What Everyone Gets Wrong

Rob Misc. Research 47 Comments

In 2007, I asked a dermatologist if low blood flow or poor circulation causes hair loss. He answered with a firm no. He told me that when he cuts into a balding scalp, it bleeds… a lot. He mentioned that the scalp is one of the most densely vascularized regions in the entire body — and as such, there’s just no way a restricted blood supply could cause androgenic alopecia (or pattern hair loss).

At first, I accepted the argument. After all, scalp tissues do have a dense capillary network. Accordingly, scalps have about ten times the blood flow of other anatomical regions. Scalps also bleed excessively during surgery… yet men and women still lose hair there.

So, maybe poor circulation or low blood flow doesn’t cause androgenic alopecia (AGA).

But at the same time, a lot of evidence contradicts with this statement.

For instance, hair requires blood, oxygen, and nutrients to grow. And this study revealed that balding scalps have 40% less oxygen than non-balding scalps. Blood carries oxygen, so presumably, balding scalp tissues also have lower blood flow…

And they do! This study demonstrated that compared to non-balding scalps, balding scalps have 2.6 times less subcutaneous blood flow! And if blood supply is what fuels hair growth, then it make sense that lower blood flow would lead to hair loss.

This concept isn’t new to most readers here. I’ve written about the hair loss-blood flow connection before. I’ve also published a paper touching on the topic. And in these writings, I tend to convey a pretty straightforward argument: that low blood flow does cause pattern hair loss.

But the truth is… I was oversimplifying things. The science is far more nuanced and complex than I suggested. In fact, it’s not entirely clear what role poor circulation has in AGA… if any at all.

This article explains why. And this time, no simplifications. We’re diving into the circulation-AGA connection and all its nuance. And just as a heads up — this article gets a little technical.

First, we’ll uncover a major study that led scientists to conclude that poor circulation doesn’t cause AGA. In other words, we’ll build the strongest opposition to the idea that reduced blood flow causes pattern hair loss. Then we’ll build the counterargument — revealing new findings that contradict a 50+ year-old belief about the blood flow-hair loss connection.

Finally, I’ll explain where I stand on the issue — and why, when it comes to reversing AGA, improving blood flow is incredibly hard. By the end, we should have gained a firm understanding of the hair cycle, how it influences scalp blood flow, where AGA morphology comes into play… and why these factors make it so hard to parcel out causation from correlation for poor circulation and AGA.

If you have any questions, please reach out in the comments!

Does low blood flow cause AGA? Maybe not.

The blood flow-AGA debate isn’t new. It’s as old as Roman times, with Julius Caesar reportedly believing his own male pattern baldness was due to poor scalp circulation. But it wasn’t until 1959 that investigators attempted to evaluate (in a scientific setting) whether this belief held merit.

The experiment was simple: using cadavers, researchers took biopsies of human scalp skin. Then, under a microscope, they examined the scalp skin’s hair follicles (and hair) and attempted to answer a simple question:

As a hair transitions into later stages of the hair cycle, what causes the degradation of that hair’s blood supply?

In reality, that’s not a simple question. But if we’re to understand the relationship between blood flow and pattern hair loss, we need to also understand the hair cycle… and why, when it comes to AGA pathology, answering this “simple” question is so important.

What is the hair cycle?

Our hairs are in a constant state of growing, shedding, or regenerating. This phenomenon is known as the hair cycle. And hair loss researchers like to think about the hair cycle in three stages: anagen (growth), catagen (resting), and telogen (shedding).

To identify the “stage” of any hair, we need to biopsy the scalp skin, look under a microscope, and answer two questions:

  1. Is the hair still growing?
  2. Is the hair still connected to its main blood supply?

And that means we need to look at our scalp skin from this angle (i.e., a biopsy):

Note in this graphic: those blue and red lines are small microvascular networks. Those networks are the main blood supply of the hair. And that seed-like cluster at the hair base? That’s called the dermal papilla.

The dermal papilla is what connects the hair follicle to its microvascular network. It’s sort of like the hair’s powerhouse. The dermal papilla takes in energy (i.e., blood, nutrient, and oxygen from the microvascular networks) and turns that energy into hair growth. It goes without saying that in the absence of a dermal papilla, hair cannot grow.

Knowing this, we can better define the three stages of the hair cycle. After all, each hair “stage” is defined by 1) whether a hair is still growing, and 2) the connection of that hair to the dermal papilla.

  1. Anagen (growing) (~85% of our scalp hair). Anagen hairs are growing, and still firmly connected to the dermal papilla.
  2. Catagen (resting) (~1% of our scalp hair). Catagen hairs are not growing, and their dermal papilla is beginning to descend away from the hair base.
  3. Telogen (shedding) (~10-15% of our scalp hair). Telogen hairs are not growing and are ready to fall out at any moment. Moreover, their dermal papilla has completely detached from the hair base. With 10-15% of our scalp hair in the telogen stage, this is why we lose 100+ hairs daily (even in the absence of pattern hair loss).

Once a telogen hair sheds, the dermal papilla regenerates and forms a new anagen hair… and the cycle repeats. In fact, here’s a graphic showing all three hair cycle stages:

 

Again: as the hair moves from anagen to catagen, the dermal papilla shrinks and descends away from the hair base… as does the hair’s blood supply.

This is important. Why? Because as the dermal papilla and blood supply shrink, so does the amount of blood pumping to the hair follicle. That means that hairs in catagen (resting) have less blood supply than hairs in anagen (growth).

Why is this relevant to AGA?

Well, when a hair begins to miniaturize during AGA, they reach a point where they become “stuck” in a catagen- or telogen-like state. For instance, according to this review, we see…

  1. Reduced hair follicle size and hair length
  2. Reduced dermal papilla size
  3. Reduced / degenerating micro-capillary networks to the dermal papilla

Thus, if we want to understand the order of events in AGA (i.e., if blood flow causes pattern hair loss), we need to understand what happens first as a hair enters into categen (resting). Specifically…

Does a hair stop growing after… or before that hair’s microvascular networks degenerate?

If hair growth stops after its blood supply degenerates, this implies reduced blood supply might’ve caused the hair to stop growing. If a hair stops growing before, this suggests reduced blood flow is not the cause of hair loss, but the effect.

This is what that 1959 study attempted to answer. Hence the researchers’ question:

What causes the reduction in blood supply as a hair enters into the catagen stage of the hair cycle?

And now we can begin to uncover the answers.

Do catagen hairs stop growing before or after their blood supply degenerates?

At first, the answer seems obvious. Let’s think about it…

Micro-capillary networks supply nutrients to the dermal papilla — the “powerhouse” of a hair follicle. If the power to that powerhouse (i.e., the blood vessels) decreases, then the output of that powerhouse (i.e., hair growth) must also decrease. So we should presume the order of events is…

  1. Capillary networks connected to the dermal papilla begin to degenerate, thus reducing nutrient transport, blood, and oxygen supply to the dermal papilla.
  2. In response, the dermal papilla shrinks to compensate for lower energy intake, and starts to descend from the hair.
  3. Eventually, the dermal papilla detaches from the hair entirely — disconnecting the hair from its powerhouse — causing the hair to stop growing.

This is a logical, well-reasoned sequence of events. And before researching AGA and hair cycle disorders, I believed it to make sense. There’s just one issue…

It’s 100% wrong. In fact, that 1959 study proved it. Shockingly, these researchers discovered — contrary to what was expected — that a hair actually stops growing before its capillary network (i.e., blood supply) degenerates.

Hair stops growing before its blood vessels degenerate.

That’s right. According to that study, the order is actually…

  1. A hair stops growing, and resultantly…
  2. The dermal papilla and capillary networks degenerate and eventually disconnect from the hair base.

This means that scalp blood flow decreases after a hair stops growing. And it bears emphasizing: this is completely unintuitive (at least to me).

Why? Let’s go back to our powerhouse analogy. Saying that a hair stops growing before its capillary networks degenerate is like saying that a box of chocolates stopped making itself so its factory workers (the dermal papilla and blood supply) could skip work the next day. It makes no sense.

And yet this is exactly what happens in our own scalps. In fact, here’s the quote from the paper:

These observations indicate that the degeneration of the blood vessels in the dermal papilla during catagen is a secondary effect and not the primary cause for cessation of hair growth.

What’s more, these findings aren’t just one-offs. They’ve been confirmed again… and again.

Which begs the question…

If a hair stops growing before its dermal papilla and blood supply degenerate, what triggers that hair to stop growing?

Luckily, these investigators identified a few culprits. In the biopsy photos, they noticed three distinct changes in a catagen hair’s surrounding tissue that directly preceded a stop in hair growth. They were:

  1. Changes to the connective tissue sheath
  2. Changes to the glassy membrane
  3. Changes to the external root sheath

Don’t worry about these new terms. All we need to know is where they are. See the below graphic (in the middle-left).

(source)

We can see the connective tissue sheath, external root sheath, and glassy membrane are all next to each other, surrounding the hair shaft. They’re known as mesodermal tissues (i.e., tissues surrounding where the hair grows).

And here’s what these investigators observed:

Right before a hair stops growing, these mesodermal tissues expand and distort. In doing so, they constrict the width of the hair shaft. This constriction pinches the hair, signaling for it to stop growing… which then signals to the dermal papilla and microvascular networks to degenerate.

Again, just to summarize the order. In the catagen phase of the hair cycle…

Mesodermal sheaths expand >> hair shaft gets pinched >> hair stops growing >> dermal papilla and blood vessels degenerate

This means that reduced blood flow comes after a hair stops growing.

And this had huge implications for AGA. Why? Because AGA-affected hairs undergo changes very similar to the ones observed in catagen (resting) and telogen (shedding) hairs. And after all, AGA-affected scalps have lower blood flow than non-balding scalps…

So… what did investigators extrapolate?

Reduced blood flow doesn’t cause AGA… AGA causes reduced blood flow.

This is why, in literature reviews, so many AGA investigators state that reduced blood flow in AGA happens after the hairs start to miniaturize. In other words, low blood flow is the effect of AGA… not the cause.

If true, this goes against everything I’ve written about AGA and poor circulation. And while I’ve always been willing to revise my beliefs in light of new information, this error would be a pretty big misstep.

However, we’ve only built the strongest opposition to the “poor circulation causes hair loss” argument. In other words, we’re still missing the other half of the debate!

And if you haven’t already noticed, there’s one major problem with the opposition’s logic…

The hair cycle and AGA are similar… but not identical.

This is a small (but important!) difference.

Early-stage AGA hairs might look nearly identical to hairs in catagen or telogen… but they aren’t.

In fact, there’s one major difference between AGA hairs versus categen or telogen hairs. And this difference is so important, we must exercise extreme caution when comparing any research from the hair cycle to pattern hair loss…

Which brings us to our counterargument.

The evidence that reduced blood flow causes pattern hair loss

We’ll start by dissecting the issues with the opposition’s argument.

Problem #1: AGA hairs start to miniaturize during anagen. Normal anagen hairs don’t.

In normal hair cycling, the size of the dermal papilla remains relatively consistent throughout the 2-7 years of the anagen (growth) phase. But in AGA anagen hairs, the size of the dermal papilla slowly, persistently degenerates.

This is odd. Remember: according to that 1959 paper, the expansion of surrounding tissue constricts a hair shaft and signals the hair to stop growing. According to all the literature, that is what stops hair growth, which then leads to the degeneration of the dermal papilla and blood supply, and eventually the shedding of a hair.

But in AGA, the dermal papilla begins shrinking prematurely… and well-before the hair stops growing. This creates a smaller, thinner, wispier hair… until the hair no longer grows at all.

This suggests that in AGA hairs, something must be prematurely constricting the hair shaft — thereby reducing the size of the hair and signaling to the dermal papilla to degenerate.

Importantly, this “something” also can’t be the normal mesodermal tissue expansion we see during catagen hair cycling. Otherwise, the AGA hair would simply enter into catagen and stop growing… rather than remain in anagen and keep trying to grow despite suboptimal conditions.

So do we see any evidence of this “something else” in AGA?

Yes. It’s called fibrosis (or scar tissue). And the tissues surrounding AGA-affected hair follicles are ridden with it.

Problem #2: AGA mesodermal tissues have scarring. Non-AGA hairs don’t.

At this point, we should clearly define two forms of mesodermal (connective tissue) thickening.

First, there’s the normal kind of connective tissue thickening. This is due to the hair cycle — the natural phenomenon we observe in catagen and telogen phases. The mesodermal sheaths expand into our hair shafts and constrict hair shaft growth space, thereby stopping hair growth and signaling to our dermal papilla and blood vessels to degenerate. This process does not lead to scarring.

Next, there’s the abnormal kind of connective tissue thickening. This isn’t due to the hair cycle. Rather, this is when excess, disorganized mesodermal tissues begin to accumulate around the hair shaft. These tissues present as disorganized collagen cross-hatchings. That’s just a fancy term for fibrosis… or in other words, scar tissue.

We see fibrosis surrounding AGA hairs in anagen (growth). And assuming those dozens of hair cycle studies hold true — i.e., that mesodermal thickening precedes a stop in hair growth and microvascular degeneration — we should assume that any accumulation of excess material around the hair shaft should interfere with hair growth… and maybe even force anagen hairs into premature miniaturization.

Fascinatingly, we see scar tissue accumulation in two locations surrounding AGA hairs: the dermal and connective tissue sheaths. And in later stages, this scar tissue creeps up to the surface — known as perifollicular fibrosis — which creates the infamous “shine” of a decades-bald scalp.

It’s most likely that the excess disorganized accumulation of mesodermal tissue (i.e., fibrosis) is what first signals an AGA hair to prematurely miniaturize… even if it’s still in its anagen phase.

Importantly, AGA-related scar tissue accumulation is chronic and progressive. Without serious intervention (i.e., removing whatever is causing the fibrosis), scar tissue continues to accumulate, leading to progressive hair follicle miniaturization — particularly the kind seen in AGA. And if enough scar tissue accumulates… hair can no longer grow.

This begs the question… if scarring in mesodermal sheaths drives AGA hair miniaturization… what causes the scarring?

Here is where things get interesting.

Inflammation causes fibrosis (scarring)

The cause of scarring is simple: inflammation. In fact, our degree of scarring in any tissue is usually equivalent to the severity and chronicity of inflammation in that tissue.

Accordingly, understanding this relationship can provide insights into the causes of scarring in AGA. In AGA, fibrosis accumulates slowly and progressively. That means that the inflammation causing fibrosis in AGA must also be 1) low-grade (i.e. barely noticeable), and 2) chronic (i.e., always present).

According to all the research in AGA pathology, this leaves us with one major culprit: chronic scalp tension.

In other body tissues, chronic tension has been shown to do three things:

  1. Provoke inflammation
  2. Reduce blood flow
  3. Increase scar tissue

And accordingly, chronic scalp tension is implicated in the pathology of pattern hair loss.

Chronic scalp tension may cause inflammation, fibrosis, and pattern hair loss

We see this relationship in Duchenne muscular dystrophy… we see it in thyroid-associated orbitopathy… we see it in AGA tissues. In fact, chronic tension not only explains why balding scalps have inflammation, but also why fibrosis accumulates in mesodermal tissues and the pattern of hair loss in men and women.

In other words, chronic scalp tension explains AGA pathology.

Diving into the details behind the AGA-scalp tension theory would turn this 5,000+ word article into a novel. If you’re interested in learning more, you can read this article here, my paper here, or wait for the upcoming article in two weeks.

For now, the only thing we need to know is one place (of many) where AGA scalp tension can originate:

The chronic, involuntary contraction of the muscles along the perimeter of our scalps.

In my interview with Dr. Freund (a hair loss researcher from the University of Toronto), he mentions that in men with AGA, the muscles surrounding the scalp are almost always chronically involuntarily contracted. And the craziest part? We can’t even tell it’s happening.

Interestingly, these muscles are connected to the underlying tissues at the tops of our scalps. So when the muscles contract, the tops of our scalps pull tightly (like a drum).

This causes two things to happen in AGA-prone scalp tissues:

  1. Blood flow reduces to balding regions
  2. Inflammation increases

Let’s take these one-by-one. After we understand these mechanisms, we’ll be able to understand why the argument, “low blood flow is just an effect of AGA” makes little to no sense.

1. How muscular contractions may reduce scalp blood flow

The blood supply for our extremities (i.e., our hands and feet) originate from one place: the heart. Our scalps are no different. And that means that the blood supplying the tops of our scalps (i.e., hair follicles) must originate from below, and must travel up.

Blood vessels develop through paths of “least resistance”. And that means that the blood vessels that support the tops of our scalps originate from below… and must pass through the muscle tissues along the perimeters of our scalps.

While researching botulinum toxin (i.e., Botox) as a treatment to relieve tension headaches, Dr. Freund noticed that his male and female patients with AGA (including himself) also had extremely tight scalp perimeter muscles.

Anatomically, when a muscle is flexed, it expands against its surrounding tissues… much like the mesodermal sheath expands against the hair shaft. And like the mesodermal expansion, chronic muscle contract also has a consequence: the pinching and compression of its blood vessel networks. Specifically, the blood vessles that supply the top parts of our scalps… the region where we suffer from pattern hair loss.

Interestingly, the investigators of this study revealed that balding scalps have 40% less transcutaneous oxygen than non-balding scalps… and postulated that the drop in oxygen levels couldn’t be due to hair cycle changes alone. And more importantly, that same study showed that when oxygen levels drop below a certain threshold, fibrosis forms… the same fibrosis we see in AGA.

Dr. Freund hypothesized that the chronic contraction of the scalp’s perimeter muscles might be the cause of this reduced blood flow. After all, this chronic muscular contraction should theoretically pinch the capillary networks which supply blood to AGA tissues, thereby constricting their flow and decreasing oxygen, blood, and nutrient levels.

So Dr. Freund set out to test his theory. He injected a group of AGA-affected men with Botox — a neuro-modifier that forces muscles to relax. He made these injections into all the muscles lining the perimeter of the scalp. And six months later, when the effects began to wear off, he brought these men back in for another round of injections.

After almost a year, the men came back in to gauge their change in hair count. The results: a 90% response rate for the treatment group… and an 18% increase in hair count in less than a year.

What does this indicate? That relaxing chronically contracted scalp muscles improves hair growth for men with AGA… and probably by reestablishing proper blood flow to the top of the scalp.

And what does that suggest? Unlike catagen hair cycling, reduced blood flow is likely a cause of pattern hair loss… not an effect.

For what it’s worth, Dr. Freund’s research has been validated again and again. And if we were to “model” these mechanisms, the order of operations for AGA onset would look like this:

Scalp muscles contract >> blood vessels constrict >> lower blood, oxygen, nutrients in AGA tissues >> fibrosis in mesodermal tissues >> mesodermal tissue expansion >> hair shaft constriction >> hair loss

But interestingly, Dr. Freund’s findings also elucidate another mechanism by which the chronic contraction of these muscles might cause AGA…

The increase of tension across the top of our scalps… which triggers a chronic inflammatory response.

2. How muscular contraction leads to chronic tension (and chronic inflammation)

Again, getting into the details here requires a separate article. But here are the highlights:

In 2015, this research team demonstrated that when muscles surrounding our scalp perimeter contract, they form a tension pattern at the top of our scalps that perfectly aligns with the pattern and progression of AGA. Here’s the model:

As we already know, chronic tension can be interpreted in the body as inflammation.

Resultantly, our bodies will try to “respond” to this inflammation by sending signaling proteins (i.e. TGF-B1) and hormones (i.e., DHT) to resolve it. But since this inflammation is tension-derived — and not injury- or infection-derived — our bodies can’t resolve it with an inflammatory response. The end-result: a chronic, low-grade attempt at resolving inflammation that can only be resolved by relieving tension.

Eventually, this chronic inflammation results in the accumulation of scar tissue. Specifically, fibrosis in mesodermal tissues. And just like mesodermal sheath expansion in the catagen phase of the hair cycle, any additional accumulation of tissue in these regions will constrict hair shaft space… leading to the progressive miniaturization of hair.

In this model, the order of operations looks like this:

Scalp muscles contract >> tension generates across top of scalp >> inflammatory response >> fibrosis in mesodermal sheath >> mesodermal tissue expansion >> hair shaft constriction alongside reduced blood flow >> hair loss.

In either model, one thing is clear: in AGA, reduced blood flow probably occurs before the hair stops growing.

This is why I believe that poor circulation is a cause of pattern hair loss. And this is why I still stand by the AGA pathology model I proposed in my paper:

Summary

End-stages of the hair cycle (i.e., catagen and telogen) share morphological similarities with early AGA progression. Resultantly, some investigators use hair cycle models to try and explain the order of events in AGA. This has been especially true for determining if reduced scalp circulation is a consequence of AGA… or a cause.

As a hair enters the catagen (resting) phase of the hair cycle, the order of operations is as follows: mesodermal tissues surrounding the hair shaft expand, thereby constricting hair shaft growth space. This stops hair growth and signals to the hair’s dermal papilla and microvascular networks to degenerate. So in the catagen phase of the hair cycle, hair growth stops before blood flow reduces… meaning that reduced blood flow is an effect of hair loss… not a cause.

AGA scalps have 2.6 times lower subcutaneous blood flow versus non-balding scalps. And since catagen hairs and early stage AGA hairs look so similar, AGA researchers have used catagen findings as a basis to argue that reduced blood flow is an effect of AGA — not a cause. In other words, these researchers surmise that reduced circulation happens after a hair disappears.

However, there are issues with this line of thinking.

The biggest problem is that early stage AGA hairs and catagen hairs are similar… but not morphologically identical. In fact, AGA hair miniaturization actually begins in the anagen (growth) phase of a hair cycle — where we begin to see slow, persistent degeneration of the dermal papilla… even as the hair attempts to keep growing.

Applying what we’ve learned from the hair cycle, this suggests that in AGA, the mesodermal tissues surrounding the hair shaft are likely prematurely expanding, and with excess material. This excess material then interferes with cross-cellular communication between the AGA hair’s connective tissue sheaths and its dermal papilla — forcing its early degeneration. Interestingly, all evidence points to this “excess material” being fibrotic material… also known as scar tissue. In the normal hair cycle, mesodermal sheath thickening reduces after a hair sheds, thereby un-pinching the hair shaft and allowing a new hair to form and grow. But in AGA, this “new” hair is thinner and wispier than the last — because the fibrotic material in the mesodermal sheath simply keeps accumulating.

Fibrotic material accumulation in the dermal sheath is likely the result of two things: 1) a chronically reduced blood supply to the top of the scalp, and 2) chronic inflammation. And there is only one likely culprit: chronic scalp tension.

Regardless of how we decide to model it, chronic scalp tension leads to a reduction in blood, oxygen, and nutrient supply to mesodermal tissues surrounding the hair shafts… thereby encouraging the accumulation of fibrosis, the constriction of hair shaft spacing, and the accidental early signaling for dermal papilla to degenerate during anagen. Eventually, this leads to AGA-related hair follicle miniaturization.

The bottom-line:

  1. AGA-related hair miniaturization is not the same as hair loss related to the hair cycle.
  2. AGA-related fibrosis likely occurs independently of the hair cycle.
  3. In AGA, reduced blood flow is likely one cause of pattern hair loss.

Any questions? You can reach me in the comments any time.

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Comments 47

    1. Post
      Author
  1. Hi Rob! First its great that you’ve posted after quite some time! I find it exciting when you create a new article almost like xmas day!

    So to the queries i have:

    1) What causes scalp muscles to be in constant contraction in the first place? And is there a link with genetics because how come we dont see this issue with scalp muscles contracting for guys with no genetic link to hair loss?

    2) What about the (sometimes) positive success of minoxidil as a blood flow agent, how does that fit within the explanation you have here?

    3) You mentioned DHT here acting as an anti-inflammatory or at least is released to deal with inflamation, are you saying DHT in this case is actually positive and that it isnt agrevating the hair follicles but instead trying to heal it?
    If that is the case, then how come you see many people gain success when they reduce serum DHT, for a lot of people reducing DHT stops or even regrows their hair.

    1. Post
      Author

      Hey Danny,

      Thanks for the kind words! And great questions.

      1. It’s really hard to say, but it’s likely due to a few factors: 1) androgens, 2) genetics, 3) scalp skull structure / suture settlement, and 4) fascia remodeling. All of these factors have feedback loops that influence the degree of 1) tension, and 2) androgen receptor density and coactivator expression — which may result in a higher propensity for certain men with AGA to have these muscles chronically contracted.

      2. I’ve long wondered this too. There’s certainly merit to increasing blood flow to the scalp. But as you’ve picked up on, absolute improvements to blood flow mean nothing. What we really want is an increase in blood that is the result of the regeneration of the microvascular networks and dermal papilla. A better way do this is probably by targeting dermal papilla stem cell expression. Wounding is a great way to do this. There are others as well (I’ll probably mention them in the upcoming articles).

      In terms of minoxidil — there are several other purported mechanisms by which minoxidil may improve AGA. Outside of improving circulation, minoxidil also has an effect on increasing prostaglandins, specifically from the prostaglandin E family. Many researchers now believe that this might be the major mechanism by which minoxidil improves AGA. So it’s likely that while minoxidil certainly improves blood flow, its main mechanism might not be that. In any case, it does help marginally to improve blood flow. For instance, rosemary oil seems to work directionally as well as minoxidil — at least according to one study — but its effects are mainly just believed to be from vasodilation. So there’s certainly benefit there.

      3. DHT is certainly implicated in AGA pathology, but paradoxically, it encourages hair growth everywhere else in our body. One way that we can actually explain this is that when DHT arrives as an anti-inflammatory agent to a tissue, but that tissue is under chronic tension (i.e., the inflammation is tension-mediated), DHT appears to induce a signaling protein called transforming growth factor beta 1 (TGFB-1). DHT + TGFB-1 is what appears to lead to scar tissue development. So this would actually explain why DHT sort of “backfires” in the scalp. DHT wants to help, but under tension, DHT lays down scar tissue.

      Along those lines, any systemic reduction in DHT (i.e., finasteride — a type II 5-alpha reductase inhibitor) should, after a certain threshold, diminish tissue DHT levels. So that’s why DHT reducers are helpful.

      Best,
      Rob

      1. Wow, good job rob. It had long been a theory of mine, after knowing syntethic DHT steroids are used for wound healing: https://www.ncbi.nlm.nih.gov/pubmed/19170590 that DHT lays down scar tissue which would causes fibrosis.
        Might I also add that excess estrogen is inflammatory as you know, but DHT antagonizes and keeps estrogen in balance.
        What you describe about blood flow is also very similar to my own conclusions.

        That’s why Taurine, which reverses fibrosis, has actually been tested to be more effective than finasteride
        Thanks

  2. Hi Rob. I bought your e book and started the massages. Did them for about 4 months as prescribed. My main problem is my vertex and was seeing thinning in that area. Although my top and front have always been thick, in the summer I noticed considerable thinning when the sun was shining down or under harsh light I could see my scalp. I hadn’t noticed it before or within the first couple of months of massaging.
    I didn’t notice any hairs being lost as I did the massages or any noticeable hair shedding on my clothes over this period.
    Could the massages cause a shock to my scalp and cause telogen effluvium? I stopped because I thought I was maybe causing problems. I now have diffuse thinning on top.
    I started rogain a few weeks ago in order to get back what I lost.
    Any suggestions?

    1. Post
      Author

      Hey Mick,

      I’m sorry to hear that you’ve experienced additional thinning since starting the massages. It’s tough to say what’s going on without a bit more information. In general, the massages should never lead to a visible increase in hair loss — particularly if minimal shedding is observed during the sessions. So I’m wondering if this is due to a) seasonal hair changes related to the hair cycle, b) the natural progression of AGA, or c) massage-induced.

      Since we shouldn’t see shock-loss of telogen effluvium associated with the massages, this suggests that maybe there will be benefit if you try to taper / reduce your massage intensity. Or just drop them for the next little while and see what happens. Also — if you’re using Rogaine, I’d recommend also adding in a 1.5mm, 192-count dermaroller once weekly. Evidence suggests that this will improve hair count 4x versus minoxidil alone. That way, we can maximize your chances of getting back on track with the hair.

      Best,
      Rob

  3. Great article! I’m looking forward to the article on the AGA-scalp tension theory! 🙂

    I think there are generally speaking two ways to look at hair loss or any health related issue. There’s the hard science that looks at very detailed aspects of the pathology and then there’s an approach that looks at the bigger picture (what general changes in the environment did happen to get you there etc, not necessarily less scientific).
    I think the scalp tension theory and specifically the arguments you laid out in your articles give a very fitting explanation and make sense regarding both approaches.

    I recently stumbled upon articles about strength training in relation to flexibility.
    For example: https://www.webmd.com/fitness-exercise/news/20100604/resistance-training-improves-flexibility-too
    It pretty much says that full range resistance training results in increased flexibility on par with (sometimes even better) stretching. “Full range” seems to be very important in contrast to chronic contraction from for example stress. So one reason why we loose flexibility in this area could be due to a decline in consumption of hard chewable foods. I think that’s really interesting and could be another piece of the chronic tension theory.

    I’d be really interested in hearing your thoughts about this. I didn’t really have the time to dig deeper into this yet unfortunately, but hopefully in the future.

    Best,
    Tim

    1. Post
      Author

      Thanks Tim!

      I think you’re on to something re: jaw development, skull structure, AGA tensile projections, etc. As we age, there’s a constant feedback loop between our skull development and mechanical stress (i.e., mechanotransduction). I hope the upcoming articles better elucidate your question! They should be ready in the next two weeks.

      Best,
      Rob

  4. So are you saying all we need to do is use botox on our scalp?

    I feel its still all about genetics at the end of the day, the genetic model of hair loss fits everything tbh, it explains why homeless men may still have their hair, it explains why fat unhealthy men still have their hair/hairline the list goes on, and there is a ton of evidence supporting it like for example even you have amazing hair, yes you was thinning but you say your dad has his hair, so for you it was probably just some health issue that you corrected with your diet approach (Thyroid etc) and as for the massages it likely just gave a bit more blood flow to the area.

    I mean come on, you see professional athletes who are extremely healthy, they dont live sedentary, have the correct nutrition for their biology, in the prime of bodily fitness and im sure they also make their bodies more ‘flexible’ which can lessen the strain from bad posture on the scalp, yet you have some of them go bald and or are balding, i can list soccer players, basketball players and im sure when you look at it their dad probably had hair loss issues, in fact a soccer player called arjen robben is completely bald and hes one of the best players in the world, but guess what his dad is exactly the same, completely bald.

    If anything dht probably travels to the scalp in response to the genes being activated by age as it is meant to do so purely from an age standpoint, like how we start getting wrinkles as we age, hair loss probably triggers in response to general aging, its just a bad gene that gets triggered by age. I mean even for myself, my dad had really thick hair at 19 same as me and he lost the majority of his at around 24/25 exactly whats happening with me.

    1. Post
      Author

      Hey Milik,

      Genetics are certainly a big factor (probably the biggest)! Genes + environmental inputs are what determine gene expression, and that’s what determines everything from how tall we are to the tensile projections at the tops of our scalps to our propensity to respond to inflammation with DHT. Because of this, it would make sense for AGA to run in the family, and affect sons at roughly the same age as it affected fathers (since skull structure, suture settlement, etc. are largely genetically determined).

      Botox injections certainly aren’t a cure-all for AGA. I wish it were that simple! Botox just goes after one target (i.e., contracted muscles) of several involved in AGA pathology.

      Best,
      Rob

      1. Hi Rob,

        Thank you for producing this research.

        I’ve read your articles on contracted scalp muscles and hair-loss.

        Are you now at a stage in which you recommend a course of action?

        Would it include botox, scalp massage, DHT inhibitors (if tolerated) and derma-rolling?

        ** Apologies if you’ve already answered this question

      2. Post
        Author

        Thanks Anonymous. It really comes down to personal preferences — i.e., finances, daily time commitment to a regimen, etc. All of what you’ve mentioned are very viable options, and certainly synergistic. In my interview with Dr. Freund, he mentioned that the lifts he would see from men doing Botox + finasteride, minoxidil, or both were sometimes 50%+ increases to hair count. But again, Botox is expensive — and finasteride always comes accompanied with caveats.

    1. Post
      Author

      Thanks Bob. It’s hard to say! It depends on your comfortability with AGA drugs, time commitments to treatment, and finances. Generally I think mechanostimulation + FDA-approved drugs are a great start, but mechanical exercises on their own also reap results. What is your current hair regimen?

    1. Post
      Author
  5. Good to see you back, Rob, though no doubt you’re busy in the background.

    So, would it be fair to assume back and sides in respect of massage are arguably most important?

    1. Post
      Author

      Hey BB — thank you! And yes. There’s certainly a few mechanisms at play with the massages. In thinning regions (the top of the scalp), we have acute wounding / stretching — which promotes growth factor expression (i.e., VEGF-A), dermal papilla stem cell proliferation, etc. Along the scalp perimeter, we have the the relaxation of chronically involuntarily tensed muscles — which improves scalp tension, blood flow, etc. The people who are getting the best results are targeting both.

  6. Huge fan Rob of your work and it is good to see you back, there seems to be quite a few people who are awaiting your response in the other articles I’ve noticed too.

    I was personally wondering because i heard it somewhere in one of the comments on another article that you were making a new updated version of the book, is there any possible dates we could have or any updates in general about upcoming things we could get excited about, perhaps that could be an added section on this website like you have the book and article section, perhaps a news section or something to keep us updated on what you’re up to these days, just a thought.

    Anyway all the best!

    1. Post
      Author

      Thanks Derek! Yes, I’m behind on comments and emails, but am making a push to catch up with everyone this week.

      I’m still working on a major update to the book, and I don’t yet know when it will be ready. Hopefully within the next two months! Otherwise, I agree with your idea idea to have a section of the site explaining what I’m currently working on. I’ll certainly add that soon (probably as part of an About Me page). Thanks for the advice!

  7. It’s interesting how you were opposed to finnasteride etc in the past but seem to be ok with it now.

    Im curious to know hows your journey going? Are the massages still working?

    1. Post
      Author

      Hey Hasan — all is well over here. Finasteride and minoxidil are certainly viable options for AGA, but it’s all context-specific. I think finasteride is over-prescribed, and oftentimes for types of hair loss that have nothing to do with androgens. You also have to weigh the potential benefits of finasteride with its risks. For instance, it’s recommended that someone not conceive while taking finasteride, and I believe the wash-out period is 1-3 months before it’s okay to start trying. Hair gains from finasteride only last as long as you continue taking it, with an expectation that anything maintained or regrown will be lost within 3-12 months after stopping its use. So, for someone trying to conceive in the near-future, finasteride is probably a bad bet. Moreover, you also have to weigh the potential for long-term side effects (brain fog, sexual dysfunction, gynecomastia, etc.) against any maintained hair. But again, finasteride / minoxidil certainly works well, and it may have synergistic effects with mechanical stimulation.

      Everything is fine on this end. I’ve personally been experimenting with little-to-no massage work to see how long results maintain in the absence of any therapy. The massages are still working, and hopefully, we should be publishing our data very soon.

      Best,
      Rob

  8. So does means that we should make a change in the protocol proposed in the book? How can we translate that into real life actions? Anyway I am in Holiday in thailand, i came from Europe and I am shedding like 300/400 hairs at day, is there any reason for it??

    1. Post
      Author

      Hey Alex,

      The current book appears to be working for most people, so as long as you’re following the demonstration video, you should be moving in the right direction. I’m also working on a book update which will get into more specifics about improving results. In terms of the shedding — this could be from any number of things, but given the context of travel, it sounds potentially telogen effluvium-related. This could be from any number of things (chronically reduced sleep / sleep quality, weight loss, a parasitic infection, gut dysbiosis, etc.). In other words, anything that chronically increases stress (and thereby cortisol).

      Best,
      Rob

  9. Great article Rob.

    Does this is indicate that nutrition and dietry approaches to AGA, will be minimal in effect ?

    We have a cause ,which going by your hypothesis could be caused by post pubertal skull bone growth causing tension , inflammation and tissue remodeling.

    A healthy diet will be minimal it seems in reversing MPB. While a mechanical approach would help significantly.

    This could explain why even healthy people can’t reverse MPB. And why unhealthy people still have hair.

    Thanks

    Kind regards
    Paz

    1. Post
      Author

      Hey Paz,

      Thank you. I think nutrition / diet certainly have a place in improving overall health and reducing systemic inflammation. But as far as improving AGA with diet / nutrition, I think we’re extremely limited. While the occurrences are less common, we still see bald indigenous men who have gone their entire lives with a diet and lifestyle the western world idolizes. My current stance is that AGA is mediated through both genetics and androgens, and is essentially a structurally-induced (and thereby localized) problem. And that’s not to say that it’s irreversible. We’ve certainly seen cases of full AGA recovery (even by accident) in the medical literature. And just as you said, while a dietary approach is likely to have a minimal effect, maybe a mechanical approach will help significantly.

      Best,
      Rob

  10. Guys. Please try these stretches:

    https://livehealthy.chron.com/stretch-head-muscles-relieve-tightness-4140.html

    After reading Rob’s article, I instantly decided to tackle the muscle tightness. Understanding that your neck and trap muscles attach on top of the scull.

    Despite my pretty typical presentation of pattern loss, I have slightly more on the right side —- interestingly, the right hand side of my neck was tighter.

    I also however have an autoimmune disorder which has fused joints in my spine – reducing mobility and most-probably blood flow for a number of reasons.

    However in some ways this just further supports a lot of Rob’s articles. I’m doing everything Rob suggests, and although its not been long enough to see results, my general health has improved.

    Thanks Rob.

  11. Excellent article, Rob. My MPB started in my late teens, coincidentally the same time when my facial structure started getting more masculine. Along with hairloss I also experienced intense itching and dandruff. Why is itching and dandruff sometimes associative with MPB? Is it because of the increased sebum triggered by androgens?

    1. Post
      Author

      Thanks Scott! And it’s hard to say where the MPB “itch” and dandruff fall into play. But there are a few things going on that might explain both.

      The first is that androgens increase sebum production, so as we enter into puberty and see a surge in androgens, we’re also going to start producing more oily scalp skin. Sebum is the food of choice for a lot of pathogenic bacteria. In fact, when certain bacteria colonize sebaceous ducts, they regulate their food supply (sebum) by producing toxic byproducts, evoking an inflammatory response (i.e., acne), which signals the body to produce even more sebum — and the cycle continues. The end-result: a lot of itching and dead skin shedding in regions that are most likely to be affected by MPB.

      Another possibility is that the dandruff is an inflammatory byproduct of the tension in scalp skin, and the dandruff is exclusively what causes the itching. We don’t yet know with certainty yet!

      Best,
      Rob

  12. Hi Rob,

    I am incredibly enthusiastic with your studies and your commitment to reverse Hair Loss. It has completely changed my perception of hairloss and motivation to do something about it. I have been doing Tom Hagerty´s exercises for 14 months and the massages for 6 weeks now. With TH exercises, I was able to reduce hairloss significantly and even get a little regrowth visible on my temples. With the massages, it is too early to say if it is leading to any progress but I continue to see new terminal hair popping at my temples. I have a few questions that I haven´t been able to find the answer to:

    1. If calcification could be partly due to pinching blood vessels, could the massages be promoting calcification?

    2. When I went hard with the massages, my scalp dried up (used to be very greasy), is this somewhat related to subcutaneous fat and hence could be bad for hair follicles?

    3. In the paper, you mention a that once there is a dettachment of the APM from a hair follicle, hair loss may be permanent. Are there other cases in which a follicle cannot be reactivated?

    4. You have mentioned several surveys with results and degree of progress, between people implementing the massages. Would it be possible for you to share the data?

    Many thanks

    1. Post
      Author

      Hey Pedro,

      Thanks for the kind words. I apologize — I’m realizing now that I haven’t replied to your previous comments in other articles. I’m a bit behind and am doing my best to catch up now. If you have any other questions, please feel free to ask.

      1. Right now, the evidence suggests that acute inflammation generated during a massage session (or microneedling) differs significantly from chronic inflammation in balding scalp tissues. Massage-mediated acute inflammation likely increases growth factors like VEGF-A and encourages stem cell proliferation for the dermal papilla (similar to a PRP session). On the other hand, chronic inflammation (the kind generated from skin tension) likely increases a different set of signaling proteins and hormones — which leads to tissue remodeling (scar tissue). The former likely helps with scar tissue, the latter likely causes it. So as of right now, I’m not worried about the massages evoking more fibrosis or calcification.

      2. This is commonly reported! It seems like after a few weeks/months of massaging, the sebaceous glands downregulate sebum production — which is probably why you noticed a less greasy scalp. I think it unrelated to subcutaneous fat.

      3. Full AGA recoveries have been documented in the medical literature — one of them happening by accident after a 78-year old bald man fell off a rocking chair, hit his head on hot coals, burned his scalp, and in the healing process, regrew his entire juvenile hairline. As a result, I think AGA recovery is possible at any Norwood stage — and regardless of whether the APM has detached. It’s just a matter of uncovering the right mechanisms!

      4. Yes! The data is currently in peer review. If the paper is accepted for publication, I’ll opt to publish it as “open access” so that everyone can benefit from the information.

      Best,
      Rob

  13. Hey Rob,

    I found an article dating back to 1997 from lifextension magazine and it mentions an explanation of an old model? Of MPB that i thought might be interesting to share and im not sure if its still relevant but here is the passage:

    ‘The latest scientific model to explain baldness involves the action of dihydrotestosterone (DHT)-the major metabolite of the male hormone testosterone. Scientists have found that excessive secretion of DHT stimulates a localized immune reaction, which, in turn, generates an inflammatory response that damages hair follicles, resulting in their miniaturization and eventual loss.

    What appears to happen is that DHT (and, perhaps, other androgenic hormones) causes the immune system to react to the hair follicles in the affected areas as foreign bodies. This is suggested by the presence of hair follicle antibodies as well as by the infiltration of immune system cells around the hair follicles of balding men and women.

    Blood vessel diseases such as atherosclerosis may also contribute to accelerated hair loss, as evidenced by the higher incidence of these diseases in balding persons.

    Successful prevention and treatment of accelerated hair loss necessitates dealing with some, if not all, of these factors involved in the process, except for the genetic component of baldness.

    The use of anti-androgens by themselves generally produces a very limited degree of hair regrowth. However, they are necessary and useful as adjuvants to other therapies such as hair-growth stimulators and oxygen free radical scavengers.

    The immune response provoked by male hormones such as DHT probably plays the most significant role in balding. Stimulated by androgens, the immune system targets hair follicles in genetically susceptible areas to cause the premature loss of hair characteristic of male pattern baldness and other forms of accelerated hair loss.

    Thus, a side effect of the immunosuppressive drug cyclosporine (which is used to prevent the rejection of transplanted organs) is scalp hair regrowth. It may be that cyclosporine is the most potent single hair regrowth agent known. But the drug causes potentially severe toxic side effects when used systemically, including kidney damage, hypertension (high blood pressure)-and even death-which precludes its use as a hair growth stimulant. However, other ways (with no potential for system toxicity) have been found to inhibit the localized immune response that leads to hair loss.

    There are many pharmaceutical agents (such as Rogaine) which can stimulate a degree of hair regrowth in some people. However, none of them alone can produce the kind of cosmetic benefits that balding people desire. What’s needed is a multi-modal approach to hair treatment that combines anti-androgens with autoimmune protective agents, oxygen free radical inhibitors, and other hair growth stimulators to halt hair loss and generate hair regrowth to a degree well beyond the abilities of single compounds.’

    This was targeted towards selling Dr Peter Proctors research and work but was wondering if the whole immune response could be an angle we haven’t looked too much at.

    I stumbled upon this when i found out that some people who had male pattern baldness actually regrew their hair back from using immunosuppresant drugs and so i thought how can that be the case if its mainly DHT and the other scalp tension issues, calcification/fibrosis etc, i haven’t see this being mentioned much but thought it interesting to share.

    All the best!

    1. Post
      Author

      Thanks James! I appreciate the comment. I know a researcher at Oxford who’s studying exactly what you’re describing. His hope is to find a target without the severe side effects of cyclosporine — maybe something localized to just the scalp skin. I’ll try to get him for an interview on the site.

      1. Wow yeh that would be amazing!

        Yeh i think its something to do with the wnt1 pathway which connects to hair growth, something called the sonic hedghog protein, i think its this pathway that scientists are looking to target, looks interesting.

  14. Rob,

    I am also a huge fan of your work. I have been following your blog for a while but it wasn’t until about 2 months ago that I began tackling hair loss seriously. I have been slowly losing hair since i was in my late twenties. I am now 37 and not ready to shave it all off yet. It was pointed out by my barber that I had lost even more hair in the span of a month (which I am sure was do to a life changing traumatic event).

    I would guess I am about a NW4. For 7 weeks, have been derma rolling with a 1.5mm roller. I had been massaging (pinching, kneading, pressing) just the crown and forehead areas as best I can (usually with a towel) as those areas are tight. Gradually, the sore spot at the top of my head went away and I think the hair fall has stopped. I do have dandruff and shampoo once a week with nizoral. I rinse daily with cold water.

    Maybe it was the timing, but this artical really spoke to me about the muscles at the periphery of the skull being contracted and tightening the skin, just like a drum. (Don’t know how I missed that in the hormone therapy piece).

    I had been neglecting to massage those muscles and only massaging the balding areas. So, 2 nights ago, I went to town on my whole head. After, I did not notice any soreness in the frontalis muscles, very light soreness in the occipital region. But when it came to the periauricular region and the temporalis muscles, holy moly was it sore. I may have over done it as I had a lump on the left side of my head which disappeared in 2 days.

    I am wondering if the periauricular region reacted that way because they were chronically tense? And contributing to the “drum head” effect? I have suffered from migraines and tension headaches my whole life.

    Anyway, keep up the stellar work! Hair loss sucks. Your work (along with some others) has given me the motivation and sparked a glimmer of hope that I can do something. I know it takes time to regrow and I am hoping I will see something here in the next couples of months. Definitely requires a lot of patience especially coming from where I am.

  15. Hey Rob,

    congratulations on another great article – I’ll read it in depth as soon as I find the time. I’d love to see an article on microneedling. I’ve seen lots of really impressive results on hair loss forums lately.

    Kind regards
    Manuel

  16. Hi Rob – I really appreciate your work on this topic and I’m sure it is changing many lives for the better since this is genuine research based analysis and it is not one of those pharma-backed rip-offs that all hair loss sufferers have gotten used to.

    I haven’t actually purchased your book but based on reading most of your articles, I started out with what I think is your protocol and I must say that the results are becoming positively obvious. I’m approaching 4 months doing the massages and almost 2+ months with the weekly dermaroller. I have had two family members say that I have noticeable hair growth and I agree! I will keep the massages going for another few months before reducing the duration since it is fairly difficult and tiring to do 40 mins each day.

    Can you please write up an article on dermarolling as you have eluded to in a few of your comment responses? I want to get your take on that in-depth. Keep up the good work and a big thank you!

  17. Hi Rob,

    Please write a detailed article on derma-rolling and derma-stamping? Everything from preparation of the scalp to use/no use of topicals, to what technique, needle length to use, etc.

    Thanks

  18. Hi rob
    I started using Rosemary oil with massage process , and I use it only for the corners of my head every night before bedtime,do you think it’s enough i use rosemary once a day? And i use it without any carrier oil

  19. Hello Rob,

    Here you are again with an great article.

    I have tried the scalp massages for two months and my scalp felt allot looser after that time. Its so time consuming that i couldnt keep it up so i stopped.

    I than started taking saw palmetto. Pumpkin seed oil and grape seed extract. My scalp tension never came back and im glad it didnt because it seems my hair finally is starting to grow stronger again.

  20. “DHT is certainly implicated in AGA pathology, but paradoxically, it encourages hair growth everywhere else in our body. ”

    Great article Rob, but with this line, I don’t feel it’s so much of a paradox.

    Scalp hair and body hair are different in the sense that scalp hair is terminal from early ages (in the absence of significant DHT), while the body hair remains vellus, only selectively becoming terminal in puberty and later life in response to DHT, with its pattern and follicular sensitivity to androgens determined by gender and genetics.

    So, it stands to reason body hair that is present as a secondary sex characteristic responds to growth from increasing levels of DHT, whereas scalp hair is terminal in children and therefore grows without requiring a response to DHT. This should make us question whether scalp hair in later life really responds in the same way to DHT as body hair does, given DHT’s primary purpose is to trigger androgenic changes, not general indiscriminate hair growth. It is not like the presence of DHT turns all vellus body hairs terminal, only where androgen sensitivity is genetically expressed.

    It seems obvious that scalp hair, not being androgenic in nature, does not require DHT to grow healthy and thick as in juveniles, and may not respond the same way as body hair follices do to DHT. I agree with your hair loss model 100%, and none of this is in contradiction to it, but I would not be surprised if it turns out DHT had no growth promoting effects on scalp hair follices, or even had a negative effect as most believe. I don’t have a reference on hand, but I do remember some study proving the link between scalp hair miniaturization and DHT, though this may of been ex vivo and away from the other scalp environment factors. Simply put, when you consider scalp hair and androgenic hair as different, with different triggering requirements, the discrepancy in the action of DHT is no longer a paradox.

  21. Dear Sir !

    Greetings,

    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.

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