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:
- Is the hair still growing?
- 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.
- Anagen (growing) (~85% of our scalp hair). Anagen hairs are growing, and still firmly connected to the dermal papilla.
- 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.
- 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…
- Reduced hair follicle size and hair length
- Reduced dermal papilla size
- 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…
- Capillary networks connected to the dermal papilla begin to degenerate, thus reducing nutrient transport, blood, and oxygen supply to the dermal papilla.
- In response, the dermal papilla shrinks to compensate for lower energy intake, and starts to descend from the hair.
- 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…
- A hair stops growing, and resultantly…
- 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.
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:
- Changes to the connective tissue sheath
- Changes to the glassy membrane
- 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).
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:
- Provoke inflammation
- Reduce blood flow
- 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:
- Blood flow reduces to balding regions
- 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.
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:
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.
- AGA-related hair miniaturization is not the same as hair loss related to the hair cycle.
- AGA-related fibrosis likely occurs independently of the hair cycle.
- 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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Rob English founded perfecthairhealth.com to share evidence-based approaches to preventing, stopping, and reversing hair loss without drugs. His interest in hair loss began in 2007, right after he was diagnosed with androgenic alopecia. Since 2014, he’s written regularly about hair loss science. He’s also published two peer-reviewed papers on androgenic alopecia and acted as a peer reviewer for journals. Feel free to browse his long-form research articles or publications throughout this site.